2 - Common Symptoms

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Tierney, Lawrence M., McPhee, Stephen J., Papadakis, Maxine A.
Current Medical Diagnosis & Treatment, 45th Edition

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Skin, Hair, & Nails

Timothy G. Berger MD

See http://www.cmdtlinks.com



Every skin disease produces a characteristic primary skin lesion. This chapter will group diseases according to the types of lesions they cause and guide the reader through the history, physical findings, and laboratory tests that discriminate among the differential diagnoses.


A detailed history is important, though in the case of skin cancer or moles (nevi) the physical examination takes precedence. Important components of a history include systemic disorders; prescription, over-the-counter, and alternative systemic and topical medications; and exposure to physical and chemical agents in the home and work environments.

Physical Examination

It is best to examine the entire skin surface, including the nails, scalp, palms, soles, and mucous membranes, in bright light. Total skin examination allows recognition of typical disease patterns and ensures that no potentially important lesions are overlooked. In examining the head for skin cancer, special attention should be paid to the lid margins, nose, ears, and lips—areas of sun exposure.


Frequently Used Treatment Measures


Soap should be used only in the axillae and groin and on the feet by persons with dry or inflamed skin. Soaking in water for 10–15 minutes before applying topical corticosteroids enhances their efficacy.


In general, topical agents used by prescription are supplied in only one strength. Exceptions include hydrocortisone (1% and 2.5%); triamcinolone acetonide cream and ointment (0.025% and 0.1%) or solution (0.1%); and fluocinolone cream, ointment, or solution (0.01%), or cream and ointment (0.025%). There is little evidence that one concentration has clinical effects that are significantly different from another. Nondermatologists should become familiar with a few agents and use them properly rather than try to master the universe of topical agents.

1. Corticosteroids

Representative topical corticosteroid creams, lotions, ointments, gels, and sprays are presented in Table 6-1. Specific indications for topical corticosteroid therapy will be discussed in the context of specific dermatologic entities. Topical corticosteroids are divided into classes based on their potency. There is little (except price) to recommend one agent over another within the same class. For a given agent, an ointment is more potent than a cream; however, ointments are generally more greasy. The potency of a topical corticosteroid may be dramatically increased by applying an occlusive dressing over the corticosteroid. At least 4 hours of occlusion is required to enhance penetration. Such dressings may include gloves, plastic wrap, or plastic occlusive suits for patients with generalized erythroderma or atopy. Caution should be used in applying topical corticosteroids to areas of thin skin (face, scrotum, vulva, skin folds). Topical corticosteroid use on the eyelids may result in glaucoma or cataracts. One may estimate the amount of topical corticosteroid needed by using the “rule of nines” (as in burn evaluation; see Figure 38-2). In general, it takes an average of 20–30 g to cover the body surface of an adult once. Systemic absorption does occur, but adrenal suppression, diabetes, hypertension, osteoporosis, and other complications of systemic corticosteroids are very rare with topical corticosteroid therapy.

2. Emollients for dry skin (“moisturizers”)

Dry skin is not related to water intake but to abnormal function of the epidermis. Many types of emollients are available. Petrolatum, mineral oil, Aquaphor, and Eucerin cream are the heaviest and best. Emollients are most effective when applied to wet skin immediately after a bath. They should be applied with the “grain” of the hairs rather than by rubbing up and down to avoid folliculitis. If the skin is too greasy after application, pat dry with a damp towel.

In some cases, lotions may be useful and are not as greasy as creams and ointments. The appearance of dry skin and ichthyosis may be improved by lactic acid products (Lac-Hydrin, U-Lactin) or glycolic acid-cotaining






lotions (Aqua Glycolic) provided no inflammation (erythema or pruritus) is present. Moisturizers that mimic the skin's normal lipids and thus feel less greasy than ointments include SBR Lipocream and Triceram cream.

Table 6-1. Useful topical dermatologic therapeutic agents.

Agent Formulations, Strengths, and Prices1 Apply Potency Class Common Indications Comments
   Hydrocortisone acetate Cream 1%:$3.60/30 g
Ointment 1%:$3.72/30 g
Lotion 1%:$20.20/120 mL
bid Low Seborrheic dermatitis.
Pruritus ani.
Not the same as hydrocortisone butyrate or valerate!
Not for poison oak!
OTC lotion (Aquinil HC).
OTC solution (Scalpicin, T Scalp).
Cream 2.5%:$8.95/30 g bid Low As for 1% hydrocortisone. Perhaps better for pruritus ani.
Not clearly better than 1%.
More expensive. Not OTC.
   Alclometasone dipropionate (Aclovate) Cream 0.05%:$20.42/15 g
Ointment 0.05%: $42.60/45 g
bid Low As for hydrocortisone. More efficacious than hydrocortisone.
Perhaps causes less atrophy.
   Desonide Cream 0.05%:$15.45/15 g
Ointment 0.05%: $40.15/60 g
Lotion 0.05%:$32.83/60 mL
bid Low As for hydrocortisone.
For lesions on face or body folds resistant to hydrocortisone.
More efficacious than hydrocortisone.
Can cause rosacea or atrophy.
Not fluorinated.
   Prednicarbate (Dermatop) Emollient cream 0.1%: $21.83/15 g
Ointment 0.1%:$21.65/15 g
bid Medium As for triamcinolone. May cause less atrophy. No generic formulations. Preservative-free.
   Triamcinolone acetonide Cream 0.1%:$3.60/15 g
Ointment 0.1%:$3.60/15 g
Lotion 0.1%:$42.44/60 mL
bid Medium Eczema on extensor areas.
Used for psoriasis with tar.
Seborrheic dermatitis and psoriasis on scalp.
Caution in body folds, face.
Economical in 0.5-lb and 1-lb sizes for treatment of large body surfaces.
Economical as solution for scalp.
Cream 0.025%:$3.00/15 g
Ointment 0.025%: $5.25/80 g
bid Medium As for 0.1% strength. Possibly less efficacy and few advantages over 0.1% formulation.
   Fluocinolone acetonide Cream 0.025%:$3.05/15 g
Ointment 0.025%: $4.20/15 g
bid Medium As for triamcinolone.  
Solution 0.01%: $11.00/60 mL bid Medium As for triamcinolone solution.  
   Mometasone furoate (Elocon) Cream 0.1%:$29.41/15 g
Ointment 0.1%:$24.30/15 g
Lotion 0.1%:$60.91/60 mL
qd Medium As for triamcinolone. Often used inappropriately on the face or in children. Not fluorinated.
   Diflorasone diacetate Cream 0.05%:$36.78/15 g
Ointment 0.05%: $51.86/30 g
bid High Nummular dermatitis.
Allergic contact dermatitis.
Lichen simplex chronicus.
   Amcinonide (Cyclocort) Cream 0.1%:$20.58/15 g
Ointment 0.1%:$30.68/30 g
bid High As for betamethasone.  
   Fluocinonide (Lidex) Cream 0.05%:$10.61/15 g
Gel 0.05%:$21.01/15 g
Ointment 0.05%: $21.25/15 g
Solution 0.05%: $27.27/60 mL
bid High As for betamethasone.
Gel useful for poison oak.
Economical generics.
Lidex cream can cause stinging on eczema.
Lidex emollient cream preferred.
   Betamethasone dipropionate (Diprolene) Cream 0.05%:$7.80/15 g
Ointment 0.05%:$9.40/15 g
Lotion 0.05%: $30.49/60 mL
bid Ultra-high For lesions resistant to high-potency steroids.
Lichen planus.
Insect bites.
Economical generics available.
   Clobetasol propionate (Temovate) Cream 0.05%:$24.71/15 g
Ointment 0.05%: $24.71/15 g
Lotion 0.05%: $53.10/50 mL
bid Ultra-high As for betamethasone dipropionate. Somewhat more potent than diflorasone.
Limited to 2 continuous weeks of use.
Limited to 50 g or less per week.
Cream may cause stinging; use “emollient cream” formulation. Generic available.
   Halobetasol propionate (Ultravate) Cream 0.05%:$34.75/15 g
Ointment 0.05%: $34.75/15 g
bid Ultra-high As for clobetasol. Same restrictions as clobetasol.
Cream does not cause stinging.
Compatible with calcipotriene (Dovonex).
   Flurandrenolide (Cordran) Tape:$47.31/80“ 3” roll
Lotion 0.05%:$45.42/60 mL
q12h Ultra-high Lichen simplex chronicus. Protects the skin and prevents scratching.
Nonsteroidal anti-inflammatory agents
   Tacrolimus2 (Protopic) Ointment 0.1%:$67.82/30 g
Ointment 0.03%: $63.46/30 g
bid N/A Atopic dermatitis. Steroid substitute not causing
atrophy or striae. Burns in ≥
40% of patients with eczema.
   Pimecrolimus2 (Elidel) Cream 1%:$56.53/30 g bid N/A Atopic dermatitis. Steroid substitute not causing atrophy or striae.
Antibiotics (for acne)
   Clindamycin phosphate Solution 1%:$12.09/30 mL
Gel 1%:$38.13/30 mL
Lotion 1%:$53.06/60 mL
Pledget 1%:$50.25/60
bid N/A Mild papular acne. Lotion is less drying for patients with sensitive skin.
   Erythromycin Solution 2%:$7.53/60 mL
Gel 2%:$24.73/30 g
Pledget 2%:$26.07/60
bid N/A As for clindamycin. Many different manufacturers.
   Erythromycin/ Benzoyl peroxide (Benzamycin) Gel:$68.60/23.3 g
Gel:$128.00/46.6 g
bid N/A As for clindamycin.
Can help treat comedonal acne.
No generics. More expensive.
More effective than other topical antibiotics.
Main jar requires refrigeration.
   Clindamycin/ Benzoyl peroxide (Benzeclin) Gel:$64.97/25 g
Gel:$122.84/50 g
bid   As for benzamycin. No generic. More effective than either agent alone.
Antibiotics (for impetigo)
   Mupirocin (Bactroban) Ointment 2%:$42.75/22 g
Cream 2%:$34.39/15 g
tid N/A Impetigo, folliculitis. Because of cost, use limited to tiny areas of impetigo.
Used in the nose twice daily for 5 days to reduce staphylococcal carriage.
   Clotrimazole Cream 1%:$5.29/15 g OTC
Solution 1%:$5.69/10 mL
bid N/A Dermatophyte and candida infections. Available OTC.
Inexpensive generic cream available.
   Miconazole Cream 2%:$2.36/30 g OTC bid N/A As for clotrimazole. As for clotrimazole.
Other imidazoles
   Econazole (Spectazole) Cream 1%:$19.27/15 g qd N/A As for clotrimazole. No generic. Somewhat more effective than clotrimazole and miconazole.
   Ketoconazole Cream 2%:$16.85/15 g qd N/A As for clotrimazole. No generic. Somewhat more effective than clotrimazole and miconazole.
   Oxiconazole (Oxistat) Cream 1%:$23.66/15 g
Lotion 1%:$39.83/30 mL
bid N/A    
   Sulconazole (Exelderm) Cream 1%:$12.56/15 g
Solution 1%:$27.05/30 mL
bid N/A As for clotrimazole. No generic. Somewhat more effective than clotrimazole and miconazole.
Other antifungals
   Butenafine (Mentax) Cream 1%:$40.27/15 g qd N/A Dermatophytes. Fast response; high cure rate; expensive. Available OTC.
   Ciclopirox (Loprox) (Penlac) Cream 0.77%:$47.13/30 g
Lotion 0.77%:$96.15/60 mL
Solution 8%:$137.46/6.6 mL
bid N/A As for clotrimazole. No generic. Somewhat more effective than clotrimazole and miconazole.
   Naftifine (Naftin) Cream 1%:$44.16/30 g
Gel 1%:$71.01/60 mL
qd N/A Dermatophytes. No generic. Somewhat more effective than clotrimazole and miconazole.
   Terbinafine (Lamisil) Cream 1%:$6.79/12 g OTC qd N/A Dermatophytes. Fast clinical response. OTC.
   Camphor/ menthol Compounded lotion (0.5% of each) bid–tid N/A Mild eczema, xerosis, mild contact dermatitis.
   Pramoxine hydrochloride (Prax) Lotion 1%:$13.33/120 mL qid N/A Dry skin, varicella, mild eczema, pruritus ani. OTC formulations (Prax, Aveeno Anti-Itch Cream or Lotion; Itch-X Gel).
By prescription mixed with 1% or 2% hydrocortisone.
   Doxepin (Zonalon) Cream 5%:$64.19/30 g qid N/A Topical antipruritic, best used in combination with appropriate topical steroid to enhance efficacy. Can cause sedation.
   Aveeno Cream, lotion, others qd–tid N/A Xerosis, eczema. Choice is most often based on personal preference by patient.
   Aqua glycolic Cream, lotion, shampoo, others qd–tid N/A Xerosis, ichthyosis, keratosis pilaris.
Mild facial wrinkles.
Mild acne or seborrheic dermatitis.
Contains 8% glycolic acid.
Available from other makers, eg, Alpha Hydrox, or generic 8% glycolic acid lotion.
May cause stinging on eczematous skin.
   Aquaphor Ointment:$7.50/50 g qd–tid N/A Xerosis, eczema.
For protection of area in pruritus ani.
Not as greasy as petrolatum.
   Carmol Lotion 10%:$8.80/180 mL
Cream 20%:$8.75/90 g
bid N/A Xerosis. Contains urea as humectant. Nongreasy hydrating agent (10%); debrides keratin (20%).
   Complex 15 Lotion:$6.48/240 mL
Cream:$4.82/75 g
qd–tid N/A Xerosis. Lotion or cream recommended for split or dry nails. Active ingredient is a phospholipid.
   DML Cream, lotion, facial moisturizer:$6.30/240 mL qd–tid N/A As for Complex 15. Face cream has sunscreen.
   Eucerin Cream:$5.10/120 g
Lotion:$5.10/240 mL
qd–tid N/A Xerosis, eczema. Many formulations made.
Eucerin Plus contains alphahydroxy acid and may cause stinging on eczematous skin.
Facial moisturizer has SPF 25 sunscreen.
   Lac-Hydrin-Five Lotion:$10.12/240 mL OTC bid N/A Xerosis, ichthyosis, keratosis pilaris. Rx product is 12%.
   Lubriderm Lotion:$5.03/300 mL qd–tid N/A Xerosis, eczema. Unscented usually preferred.
   Neutrogena Cream, lotion, facial moisturizer:$7.39/240 mL qd–tid N/A Xerosis, eczema. Face cream has titaniumbased sunscreen.
   SBR Lipocream Cream:$7.43/30 g qd-tid N/A Xerosis, eczema. Less greasy but effective moisturizer.
   Triceram Cream Cream:$30.00/3.4-oz tube bid N/A Xerosis, eczema. Contains ceramide; anti-inflammatory and non-greasy moisturizer.
   U-Lactin Lotion:$7.13/240 mL qd N/A Hyperkeratotic heels. Moisturizes and removes keratin.
1Average wholesale price (AWP, for AB-rated generic when available) for quantity listed. AWP may not accurately represent the actual pharmacy cost because wide contractual variations exist among institutions. Source: Red Book Update, Vol. 24, No. 4, May 2005.
2 Topical tacrolimus and pimecrolimus should only be used when other topical treatments are ineffective. Treatment duration should be limited to an area and be as brief as possible. Treatment with these agents should be avoided in persons with known immunosuppression, HIV infection, bone marrow and organ transplantation, lymphoma, at high risk for lymphoma, and those with a prior history of lymphoma.
OTC = over-the-counter; N/A = not applicable.

3. Drying agents for weepy dermatoses

If the skin is weepy from infection or inflammation, drying agents may afford relief. The best drying agent is water, and repeated compresses may be applied for 15–30 minutes alone or with aluminum salts (Burow's solution, Domeboro tablets) or colloidal oatmeal (Aveeno). Shake lotions (eg, starch or calamine lotions) and powders (especially if the process is acute) may result in messy crusts and are seldom used by dermatologists.

4. Topical antipruritics

Lotions that contain 0.5% each of camphor and menthol (Sarna) are effective for mild pruritic dermatoses. Pramoxine hydrochloride, 1% cream or lotion, with or without 0.5% menthol, is an effective antipruritic agent (eg, Prax, PrameGel, Aveeno Anti-Itch lotion). Hydrocortisone, 1% or 2.5%, may be incorporated for its anti-inflammatory effect (Pramosone cream, lotion, or ointment). Doxepin cream 5% may reduce pruritus due to eczematous dermatoses. Drowsiness may occur. Pramoxine and doxepin are most effective when applied with topical corticosteroids. Monoamine oxidase inhibitors should be discontinued at least 2 weeks before treatment with doxepin.

5. Systemic antipruritic drugs

a. Antihistamines

H1 blockers are the agents of choice for pruritus when due to histamine, such as in urticaria. Otherwise, they appear to relieve pruritus only by their sedating and not their antihistamine effects. Except in the case of urticaria, nonsedating antihistamines are of little or no value in inflammatory skin diseases such as atopic dermatitis and are rarely indicated.

Hydroxyzine 25–50 mg nightly is typically used for its sedative effect in pruritic diseases. Sedation can limit daytime use. The least sedating antihistamines are loratadine and famotidine. Cetirizine causes drowsiness in about 15% of patients. Some antidepressants, such as doxepin, mirtazapine, and paroxetine can be effective antipruritics.

b. Systemic corticosteroids

(See Chapter 26.)

Clarke P: Why am I so itchy? Aust Fam Physician 2004;33:489.

Lonsdale-Eccles A et al: Treatment of pruritus with systemic disorders in the elderly: a review of the role of new therapies. Drugs Aging 2003;20:197.

Yosipovitch G et al: Practical guidelines for relief of itch. Dermatol Nurs 2004;16:325.


Protection from ultraviolet light should begin at birth but will reduce the incidence of actinic keratoses and some nonmelanoma skin cancers when initiated at any age. The best protection is shelter, but protective clothing, avoidance of direct sun exposure during the peak hours of the day, and the assiduous use of chemical sunscreens are important.

A number of highly effective sunscreens are available in cream, lotion, and nongreasy gel and liquid formulations. Fair-complexioned persons should use a sunscreen with an SPF (sun protective factor) of at least 15 and preferably 30–40 every day. For those who are sensitive to PABA (p-aminobenzoic acid), PABA-free formulations are available. Sunscreens with high SPF values (> 30) afford some protection against UVA as well as UVB light exposure and may be helpful in managing photosensitivity disorders. Physical blockers (titanium dioxide and zinc oxide) are available in vanishing formulations. Aggressive sunscreen use should be accompanied by vitamin D supplementation in persons at risk for osteopenia (eg, organ transplant recipients).

Jorgensen CM: Scientific recommendations and human behaviour: sitting out in the sun. Lancet 2002;360:351.

Vatour LM et al: Long-term fracture risk following renal transplantation: a population-based study. Osteoporos Int 2004;15:160.

Complications of Topical Dermatologic Therapy

Complications of topical therapy can be largely avoided. They fall into several categories:


Of the topical antibiotics, neomycin and bacitracin have the greatest potential for sensitization. Diphenhydramine, benzocaine, vitamin E, aromatic essential oils, and bee pollen are potential sensitizers in topical medications. Preservatives and even the topical steroids themselves can cause allergic contact dermatitis.


Preparations of tretinoin, benzoyl peroxide, and other acne medications should be applied sparingly to the skin. Sunscreens may cause irritation or an acne-like eruption.


Drugs may be absorbed through the skin, especially through broken or inflamed skin, or from under occlusive dressings. Notable examples of topical drugs to be avoided in pregnancy include podophyllum resin, and tretinoin (Retin-A). Consult a pharmacology reference source when prescribing medications for pregnant or nursing women.


Topical corticosteroids may induce acne-like lesions on the face (steroid rosacea) and atrophic striae in body folds.



Dermatologic diseases will be discussed according to the types of lesions they cause. Therefore, in order to make a diagnosis, it is best to (1) focus on the type of individual lesion the patient exhibits; (2) choose the morphologic category the lesions seem to fit; and then (3) identify the specific features of the history, physical examination, and laboratory tests that will establish the diagnosis.

The major morphologic types of skin lesion are listed in Table 6-2 along with the disorders with which they are most prominently associated. Miscellaneous skin, hair, and nail disorders and drug eruptions are discussed at the end of the chapter.


Deaths from malignant melanoma are prevented by early diagnosis followed by excision. The nondermatologist clinician must be able to evaluate pigmented lesions and appropriately refer for evaluation all potential malignant melanomas. In order to avoid missing some malignant melanomas, it is understood that many patients will be referred for what ultimately prove to be benign lesions.

Table 6-2. Morphologic categorization of skin lesions and diseases.

Pigmented Freckle, lentigo, seborrheic keratosis, nevus, blue nevus, halo nevus, dysplastic nevus, melanoma
Scaly Psoriasis, dermatitis (atopic, stasis, seborrheic, chronic allergic contact or irritant contact), xerosis (dry skin), lichen simplex chronicus, tinea, tinea versicolor, secondary syphilis, pityriasis rosea, discoid lupus erythematosus, exfoliative dermatitis, actinic keratoses, Bowen's disease, Paget's disease, intertrigo
Vesicular Herpes simplex, varicella, herpes zoster, dyshidrosis (vesicular dermatitis of palms and soles), vesicular tinea, dermatophytid, dermatitis herpetiformis, miliaria, scabies, photosensitivity
Weepy or encrusted Impetigo, acute contact allergic dermatitis, any vesicular dermatitis
Pustular Acne vulgaris, acne rosacea, folliculitis, candidiasis, miliaria, any vesicular dermatitis
Figurate (“shaped”) erythema Urticaria, erythema multiforme, erythema migrans, cellulitis, erysipelas, erysipeloid, arthropod bites
Bullous Impetigo, blistering dactylitis, pemphigus, pemphigoid, porphyria cutanea tarda, drug eruptions, erythema multiforme, toxic epidermal necrolysis
Papular Hyperkeratotic: warts, corns, seborrheic keratoses
Purple-violet: lichen planus, drug eruptions, Kaposi's sarcoma
Flesh-colored, umbilicated: molluscum contagiosum
Pearly: basal cell carcinoma, intradermal nevi
Small, red, inflammatory: acne, miliaria, candidiasis, scabies, folliculitis
Pruritus1 Xerosis, scabies, pediculosis, bites, systemic causes, anogenital pruritus
Nodular, cystic Erythema nodosum, furuncle, cystic acne, follicular (epidermal) inclusion cyst
Photodermatitis (photodistributed rashes) Drug, polymorphic light eruption, lupus erythematosus
Morbilliform Drug, viral infection, secondary syphilis
Erosive Any vesicular dermatitis, impetigo, aphthae, lichen planus, erythema multiforme
Ulcerated Decubiti, herpes simplex, skin cancers, parasitic infections, syphilis (chancre), chancroid, vasculitis, stasis, arterial disease
1Not a morphologic class but included because it is one of the most common dermatologic presentations.

In general, a benign mole is a small (< 6 mm), wellcircumscribed lesion with a well-defined border and a single shade of pigment from beige or pink to dark brown. The physical examination must take precedence over the history, though a reliable history that a lesion has been present without change for decades is obviously a comfort.

Suspicious moles have an irregular notched border where the pigment appears to be leaking into the normal surrounding skin; the topography may be irregular, ie, partly raised and partly flat. Color variegation is present, and colors such as pink, blue, gray, white, and black are indications for referral. The American Cancer Society has proposed the mnemonic “ABCD = Asymmetry, Border irregularity, Color variegation, and Diameter greater than 6 mm.” “E” for Evolution can be added. The history of a changing mole (evolution) is the single


most important historical reason for close evaluation and possible referral. Bleeding and ulceration are ominous signs. A mole that stands out from the patient's other moles deserves special scrutiny, “ugly duckling sign.” A patient with a large number of moles is statistically at increased risk for melanoma and deserves careful and periodic examination, particularly if the lesions are atypical. Referral of suspicious pigmented lesions is always appropriate.

Moles have a normal natural history. In the patient's first decade of life, moles often appear as flat, small, brown lesions. They are called junctional nevi because the nevus cells are at the junction of the epidermis and dermis. Over the next 2 decades, these moles grow in size and often become raised, reflecting the appearance of a dermal component, giving rise to compound nevi. Moles may darken and grow during pregnancy. As white patients enter their seventh and eighth decades, most moles have lost their junctional component and dark pigmentation and undergo fibrosis or other degenerative changes. Still, at every stage of life, normal moles should be well-demarcated, symmetric, and uniform in contour and color.

Abbasi NR et al: Early diagnosis of cutaneous melanoma: Revisiting the ABCD criteria. JAMA 2004;292:2771.


The management of small congenital nevi—less than a few centimeters in diameter—is controversial. The vast majority will never become malignant, but some experts feel that the risk of melanoma in these lesions may be somewhat increased. Since 1% of whites are born with these lesions, management should be conservative and excision advised only for lesions in cosmetically nonsensitive areas where the patient cannot easily see the lesion and note any suspicious changes. Excision should be considered for congenital nevi whose contour (bumpiness, nodularity) or color (different shades) makes it difficult for examiners to note early signs of malignant change. Giant congenital melanocytic nevi (> 5% body surface area [BSA]) are at greater risk for development of melanoma, and surgical removal in stages is often recommended.


The term “atypical nevus” or “atypical mole” has supplanted “dysplastic nevus.” The diagnosis of atypical moles is made clinically and not histologically, and moles should be removed only if they are suspected to be melanomas. Clinically, these moles are large (> 5 mm in diameter), with an ill-defined, irregular border and irregularly distributed pigmentation. It is estimated that 5–10% of the United States population have one or more atypical nevi. Studies have defined an increased risk of melanoma in the following populations: patients with 50 or more nevi with one or more atypical moles and one mole at least 8 mm or larger, and patients with a few to many definitely atypical moles. These patients deserve education and regular (usually every 6–12 months) follow-up. Kindreds with familial melanoma (numerous atypical nevi and a strong family history) deserve even closer attention, as the risk of developing single or even multiple melanomas in these individuals approaches 50% by age 50.

Naeyaert JM et al: Clinical practice. Dysplastic nevi. N Engl J Med 2003;349:2233.


Blue nevi are small, slightly elevated, and blue-black lesions. They are common in persons of Asian descent, and an individual patient may have several of them. If present without change for many years, they may be considered benign, since malignant blue nevi are rare. However, blue-black papules and nodules that are new or growing must be evaluated to rule out nodular melanoma.


Freckles (ephelides) and lentigines are flat brown spots. Freckles first appear in young children, darken with ultraviolet exposure, and fade with cessation of sun exposure. In adults, depending on the fairness of the complexion, flat brown spots (lentigines), often with sharp borders, gradually appear in sun-exposed areas, particularly the dorsa of the hands. They do not fade with cessation of sun exposure. They should be evaluated like all pigmented lesions: If the pigmentation is homogeneous and they are symmetric and flat, they are most likely benign. Solar lentigines, so-called liver spots, can be treated with topical 0.1% tretinoin, 2% 4-hydroxyanisole with tretinoin 0.01% (Solage), laser therapy, and cryotherapy.

Chan HH et al: The use of lasers and intense pulsed light sources of the treatment of primary lesions. Skin Therapy Lett 2004;9:5.

Ortonne JP et al: Safety and efficacy of combined use of 4-hydroxyanisole (mequinol) 2%/tretinoin 0.01% solution and sunscreen in solar lentigines. Cutis 2004,74:261.


Seborrheic keratoses are benign plaques, beige to brown or even black, 3–20 mm in diameter, with a velvety or warty surface. They appear to be stuck or pasted onto the skin. They are common—especially in the elderly—and may be mistaken for melanomas or other types of cutaneous neoplasms. Although they may be frozen with liquid nitrogen or curetted if they itch or are inflamed, no treatment is needed.

Herron MD et al: Seborrheic keratoses: a study comparing the standard cryosurgery with topical calcipotriene, topical tazarotene, and topical imiquimod. Int J Dermatol 2004;43:300.




  • May be flat or raised.

  • Should be suspected in any pigmented skin lesion with recent change in appearance.

  • Examination with good light may show varying colors, including red, white, black, and bluish.

  • Borders typically irregular.

General Considerations

Malignant melanoma is the leading cause of death due to skin disease. There were 55,000 cases of melanoma in the United States in 2004, with 7900 deaths. One in four cases of melanoma occur before the age of 40. Melanoma is the most common cancer of women between the ages of 25 and 29 and the second most common cause in women ages 30–34. Overall survival for melanomas in whites rose from 60% in 1960–1963 to 85% in 1983–1990, due primarily to earlier detection of lesions.

Tumor thickness is the single most important prognostic factor. Ten-year survival rates—related to thickness in millimeters—are as follows: < 1 mm, 95%; 1–2 mm, 80%; 2–4 mm, 55%; and > 4 mm, 30%. With lymph node involvement, the 5-year survival rate is 30%; with distant metastases, it is less than 10%. More accurate prognoses can be made on the basis of site, histologic features, and gender of the patient.

Clinical Findings

Primary malignant melanomas may be classified into various clinicohistologic types, including lentigo maligna melanoma (arising on sun-exposed skin of older individuals); superficial spreading malignant melanoma (the most common type, occurring in two-thirds of individuals developing melanoma); nodular malignant melanoma; acral-lentiginous melanomas (arising on palms, soles, and nail beds); malignant melanomas on mucous membranes; and miscellaneous forms such as amelanotic (nonpigmented) melanoma and melanomas arising from blue nevi (rare) and congenital nevi.

While superficial spreading melanoma is largely a disease of whites, persons of other races are at risk for other types of melanoma, particularly acral lentiginous melanoma. These occur as dark, sometimes irregularly shaped lesions on the palms and soles and as new, often broad and solitary, darkly pigmented longitudinal streaks in the nails. Acral lentiginous melanoma may be a difficult diagnosis because benign pigmented lesions of the hands, feet, and nails occur commonly in more darkly pigmented persons and clinicians may hesitate to biopsy the palms, soles, and nail beds. As a result, the diagnosis is often delayed until the tumor has become clinically obvious and histologically thick. Clinicians should give special attention to new or changing lesions in these areas.

Melanomas vary from macules to nodules. Variegation of color from flesh tints to pitch black and a frequent admixture of white, blue, purple, and red may occur. The border tends to be irregular, and growth may be rapid or indolent. Melanomas are often larger than 6 mm. Again, one should refer lesions based on a suspicion of melanoma rather than delay until the diagnosis is certain. Dermoscopy—use of a special magnifying device to evaluate pigmented lesions—helps select suspicious lesions that require biopsy. In experienced hands, the specificity is 85% and the sensitivity 95%.


Treatment of melanoma consists of excision. After histologic diagnosis, the area is usually reexcised with margins dictated by the thickness of the tumor. Thin low-risk and intermediate-risk tumors require only conservative margins of 1–3 cm. More specifically, surgical margins of 0.5 cm for melanoma in situ and 1 cm for lesions less than 1 mm in thickness are recommended.

Sentinel lymph node biopsy (selective lymphadenectomy) using preoperative lymphoscintigraphy and intraoperative lymphatic mapping is effective for staging melanoma patients with intermediate risk without clinical adenopathy and is recommended for all patients with lesions over 1 mm in thickness or with high-risk histologic features. α-Interferon and vaccine therapy may reduce recurrences in patients with high-risk melanomas. Referral of intermediate-risk and high-risk patients to centers with expertise in melanoma is strongly recommended.

Bafounta M et al: Is dermoscopy (epiluminescence microscopy) useful for the diagnosis of melanoma? Arch Dermatol 2001;137:1343.

Cochran AJ et al: Update on lymphatic mapping and sentinel node biopsy in the management of patients with melanocytic tumours. Pathology 2004;36:478.

McCarthy WH: The Australian experience in sun protection and screening for melanoma. J Surg Oncol 2004;86:236.

Tsao H et al: Management of cutaneous melanoma. N Engl J Med 2004;351:998.




  • Pruritic, exudative, or lichenified eruption on face, neck, upper trunk, wrists, and hands and in the antecubital and popliteal folds.

  • P.95

  • Personal or family history of allergic manifestations (eg, asthma, allergic rhinitis, atopic dermatitis).

  • Tendency to recur.

General Considerations

Atopic dermatitis looks different at different ages and in people of different races. Because most patients have scaly dry skin at some point, this disease is being discussed under scaly dermatoses. However, acute flares may present with red patches that are weepy, shiny, or lichenified (ie, thickened, with more prominent skin markings) and plaques and papules. Diagnostic criteria for atopic dermatitis must include pruritus, typical morphology and distribution (flexural lichenification in adults), and a tendency toward chronic or chronically relapsing dermatitis. Also helpful are (1) a personal or family history of atopic disease (asthma, allergic rhinitis, atopic dermatitis), (2) xerosis-ichthyosis, (3) facial pallor with infraorbital darkening, (4) elevated serum IgE, (5) fissures under the ear lobes, (6) a tendency toward nonspecific hand dermatitis, (7) a tendency toward repeated skin infections, and (8) nipple eczema.

Clinical Findings


Itching may be severe and prolonged. Rough, red patches usually without the thickening and discrete demarcation of psoriasis affect the face, neck, and upper trunk (“monk's cowl”). The bends of the elbows and knees are involved. In chronic cases, the skin is dry, leathery, and lichenified. Pigmented persons tend to present with a papular eruption, and poorly demarcated hypopigmented patches (pityriasis alba) are commonly seen on the cheeks and extremities. In black patients with severe disease, pigmentation may be lost in lichenified areas.


Food allergy is an uncommon cause of flares of atopic dermatitis in adults. Blinded food challenges are the most reliable method of diagnosing suspected food allergy. Radioallergosorbent tests (RASTs) or skin tests may suggest dust mite allergy. Eosinophilia and increased serum IgE levels may be present but are nonspecific.

Differential Diagnosis

Atopic dermatitis must be distinguished from seborrheic dermatitis (less pruritic, frequent scalp and face involvement, greasy and scaly lesions, and quick response to therapy). Contact dermatitis and impetigo may be in the differential, especially for hyperacute, weepy flares of atopic dermatitis (although typically these diseases do not have a chronic course and characteristic distribution). Patients with active lesions are almost always colonized with Staphylococcus aureus, and impetiginization of atopic skin should be considered and treated when an acute flare is present.


Treatment is most effective if the patient is instructed about the general principles of skin care and exactly how to use medications.


Atopic patients have hyperirritable skin. Anything that dries or irritates the skin will potentially trigger dermatitis. Atopic individuals are sensitive to low humidity and often get worse in the winter, when the air is dry. Adults with atopic disorders should not bathe more than once daily. Soap should be confined to the armpits, groin, scalp and feet. Washcloths and brushes should not be used. Soaps should not be drying, and Dove, Eucerin, Aveeno, Basis, Alpha Keri, Purpose, and other soaps or cleansers, such as Cetaphil or Aquanil, may be recommended. After rinsing, the skin should be patted dry (not rubbed) and then immediately—within three minutes—covered with a thin film of an emollient such as Aquaphor, Eucerin, Vaseline, or a corticosteroid as needed. Triceram cream, a therapeutic moisturizer, will reduce inflammation as well as moisturize without a greasy or occlusive feel. It is much more expensive than traditional moisturizers. Atopic patients may be irritated by scratchy fabrics, including wools and acrylics. Cottons are preferable, but synthetic blends also are tolerated. Other triggers of eczema in some patients include sweating, ointments, hot bathing, and animal danders.

To determine the potential effect of foods, the patient may eliminate one food at a time for several months and monitor the severity of the disease. Dairy products and wheat are the most common offenders. Foods that are a problem typically cause itching within minutes to a few hours after ingestion.


Corticosteroids should be applied sparingly to the dermatitis twice to four times daily and rubbed in well. Their potency should be appropriate to the severity of the dermatitis. In general, one should begin with triamcinolone 0.1% or a stronger corticosteroid then taper to hydrocortisone or another slightly stronger mild corticosteroid (Aclovate, Desonide). It is vital that patients taper corticosteroids and substitute emollients when the dermatitis clears to avoid the side effects of corticosteroids. Tapering is also important to avoid rebound flares of the dermatitis that may follow their abrupt cessation. Doxepin cream 5% may be used up to four times daily and is best applied simultaneously with the topical corticosteroid. Stinging and drowsiness occur in 25%. Tacrolimus ointment (Protopic


0.03% or 0.1%) and pimecrolimus ointment (Elidel 1%) can be effective in managing atopic dermatitis when applied twice daily. Burning on application occurs in about 50% of patients using Protopic and in 10–25% of Elidel users, but it may resolve with continued treatment. These medications do not appear to cause skin atrophy, striae, or other topical corticosteroid-associated side effects and are safe for application on the face and even the eyelids.

The US Food and Drug Administration (FDA) has ordered a black box warning for both topical tacrolimus and pimecrolimus due to concerns about the development of T-cell lymphoma. The agents should be used sparingly and only when less expensive corticosteroids cannot be used. Tacrolimus and pimecrolimus should be avoided in patients at high risk for lymphoma (ie, those with HIV, iatrogenic immunosuppression, prior lymphoma). The treatment of atopic dermatitis is dictated by the stage of the dermatitis.

1. Acute weeping lesions

Use water or aluminum subacetate solution (Domeboro tablets, one in a pint of cool water) or colloidal oatmeal (Aveeno; dispense one box, and use as directed on box) as soothing or astringent soaks, baths, or wet dressings for 10–30 minutes two to four times daily. Lesions on extremities particularly may be bandaged for protection at night. Corticosteroid lotions or creams are preferred to ointments for this stage. Use high-potency corticosteroids after bathing but spare the face and body folds. Tacrolimus may not be tolerated at this stage. Systemic corticosteroids may be required (see below).

2. Subacute or scaly lesions

At this stage, the lesions are dry but still red and pruritic. Midto highpotency corticosteroids in ointment form should be continued until scaling and elevated skin lesions are cleared and itching is decreased substantially. At that point, patients should begin a 2to 4-week taper from twice-daily to daily to alternate-day dosing with topical corticosteroids to reliance on emollients, with occasional use of corticosteroids on specific itchy areas. Instead of tapering the frequency of usage of a more potent corticosteroid, it may be preferable to switch to a low-potency corticosteroid. Tacrolimus and pimecrolimus are more expensive alternatives and may be added if corticosteroids cannot be stopped to avoid the complications of long-term topical corticosteroid use.

3. Chronic, dry, lichenified lesions

Thickened and usually well-demarcated, they are best treated with high-potency to ultra-high-potency corticosteroid ointments. Nightly occlusion for 2–6 weeks may enhance the initial response. Occasionally, adding tar preparations such as LCD (liquor carbonis detergens) 10% in Aquaphor or 2% crude coal tar may be beneficial.

4. Maintenance treatment

Once symptoms have improved, constant application of effective moisturizers is recommended to prevent flares. In patients with moderate disease, weekend only use of topical corticosteroids can prevent flares.


Systemic corticosteroids are indicated only for severe acute exacerbations. Oral prednisone dosages should be high enough to suppress the dermatitis quickly, usually starting with 40–60 mg daily for adults. The dosage is then tapered to nil over a period of 2–4 weeks. Owing to the chronic nature of atopic dermatitis and the side effects of chronic systemic corticosteroids, long-term use of these agents is not recommended for maintenance therapy. Classic antihistamines may relieve severe pruritus. Hydroxyzine, diphenhydramine, or doxepin may be useful—the dosage increased gradually to avoid drowsiness. Fissures, crusts, erosions, or pustules indicate staphylococcal infection clinically. Therefore, antistaphylococcal antibiotics given systemically—such as dicloxacillin or first-generation cephalosporins— may be helpful in management and are often used during flares. Phototherapy can be an important adjunct for severely affected patients, and the properly selected patient with recalcitrant disease may benefit greatly from therapy with UVB with or without coal tar, UVA, or PUVA (psoralen plus ultraviolet A). Oral cyclosporine or azathiopurine may be used for the most severe and recalcitrant cases.

Complications of Treatment

The clinician should monitor for skin atrophy. Eczema herpeticum, a generalized herpes simplex infection manifested by monomorphic vesicles, crusts, or erosions superimposed on atopic dermatitis or other extensive eczematous processes, is treated successfully with oral acyclovir, 200 mg five times daily, or intravenous acyclovir in a dose of 10 mg/kg intravenously every 8 hours (500 mg/m2 every 8 hours). Tacrolimus and pimecrolimus increase the risk of eczema herpeticum.

Smallpox vaccination is absolutely contraindicated in patients with atopic dermatitis or a history thereof because of the risk of eczema vaccinatum. Generalized vaccinia may develop in patients with atopic dermatitis who have contact with recent vaccine recipients who still have pustular or crusted vaccination sites. Eczema vaccinatum and generalized vaccinia are indications for vaccinia immune globulin.


Atopic dermatitis runs a chronic or intermittent course. Affected adults may have only hand dermatitis. Poor prognostic factors for persistence into adulthood in atopic dermatitis include onset early in childhood, early generalized disease, and asthma. Only 40–60% of these patients have lasting remissions.

Leung DY et al: Atopic dermatitis. Lancet 2003;361:151.

Roos TC et al: Recent advances in treatment strategies for atopic dermatitis. Drugs 2004;64:2639.


Williams HC: Twice-weekly topical corticosteroid therapy may reduce atopic dermatitis relapses. Arch Dermatol 2004;140:1151.

LICHEN SIMPLEX CHRONICUS (Circumscribed Neurodermatitis)


  • Chronic itching and scratching.

  • Lichenified lesions with exaggerated skin lines overlying a thickened, well-circumscribed scaly plaque.

  • Predilection for nape of neck, wrists, external surfaces of forearms, lower legs, scrotum, and vulva.

General Considerations

Lichen simplex chronicus represents a self-perpetuating scratch-itch cycle.

Clinical Findings

Intermittent itching incites the patient to scratch the lesions. Itching may be so intense as to interfere with sleep. Dry, leathery, hypertrophic, lichenified plaques appear on the neck, ankles, perineum, or almost anywhere. The patches are rectangular, thickened, and hyperpigmented. The skin lines are exaggerated.

Differential Diagnosis

This disorder can be differentiated from plaque-like lesions such as psoriasis (redder lesions having whiter scales on the elbows, knees, and scalp and nail findings), lichen planus (violaceous, usually smaller polygonal papules), and nummular (coin-shaped) dermatitis. Lichen simplex chronicus may complicate chronic atopic dermatitis.


For lesions in extra-genital regions, clobetasol, halobetasol, diflorasone, and betamethasone dipropionate are effective without occlusion and are used twice daily for several weeks. In some patients, flurandrenolide (Cordran) tape may be more effective, since it prevents scratching and rubbing of the lesion. These superpotent corticosteroids are probably the treatment of choice but must be used with careful follow-up to avoid local side effects. The injection of triamcinolone acetonide suspension (5–10 mg/mL) into the lesions may occasionally be curative. Use of tars, such as 10% LCD (liquor carbonis detergens) with topical corticosteroids, or continuous occlusion with a flexible hydrocolloid dressing for 7 days at a time for 1–2 months, may also be helpful. The area should be protected and the patient encouraged to become aware of when he or she is scratching. For genital lesions, see the section Pruritus Ani.


The disease tends to remit during treatment but may recur or develop at another site.



  • Silvery scales on bright red, well-demarcated plaques, usually on the knees, elbows, and scalp.

  • Nail findings including pitting and onycholysis (separation of the nail plate from the bed).

  • Mild itching (usually).

  • May be associated with psoriatic arthritis.

  • Histopathology is not often useful and can be confusing.

General Considerations

Psoriasis is a common benign, chronic inflammatory skin disease with a genetic basis. Injury or irritation of normal skin tends to induce lesions of psoriasis at the site (Koebner's phenomenon). Psoriasis has several variants—the most common is the plaque type. Eruptive (guttate) psoriasis consisting of myriad lesions 3–10 mm in diameter occurs occasionally after streptococcal pharyngitis. Rarely, grave, occasionally lifethreatening forms (generalized pustular and erythrodermic psoriasis) may occur. Plaque type or extensive erythrodermic psoriasis with abrupt onset may accompany HIV infection.

Clinical Findings

There are often no symptoms, but itching may occur. Although psoriasis may occur anywhere, the scalp, elbows, knees, palms and soles, and nails should be examined. The lesions are red, sharply defined plaques covered with silvery scales. The glans penis and vulva may be affected. Occasionally, only the flexures (axillae, inguinal areas) are involved. Fine stippling (“pitting”) in the nails is highly suggestive of psoriasis. Psoriatics often have a pink or red intergluteal fold. Not all patients have findings in all locations, but the occurrence of a few may help make the diagnosis when other lesions are not typical. Some patients have mainly hand or foot dermatitis and only minimal findings elsewhere. There may be associated arthritis


that is most commonly distal and oligoarticular, although the rheumatoid variety with a negative rheumatoid factor may occur.

Differential Diagnosis

The combination of red plaques with silvery scales on elbows and knees, with scaliness in the scalp or nail findings, is diagnostic. Psoriasis lesions are well demarcated and affect extensor surfaces—in contrast to atopic dermatitis, with poorly demarcated plaques in flexural distribution. In body folds, scraping and culture for candida and examination of scalp and nails will distinguish psoriasis from intertrigo and candidiasis. Dystrophic changes in nails may simulate onychomycosis, but again, the general examination combined with a potassium hydroxide (KOH) or fungal culture will be valuable in diagnosis. The cutaneous features of reactive arthritis (Reiter's syndrome) mimic psoriasis.


There are many therapeutic options in psoriasis to be chosen according to the extent and severity of disease and with a clear understanding of the risks and benefits of therapy. Certain drugs, such as β-blockers, antimalarials, statins, and lithium, may flare or worsen psoriasis.


For many patients, the easiest regimen is to use a highpotency to ultra-high-potency topical corticosteroid cream or ointment. It is best to restrict the ultra-highpotency corticosteroids to 2–3 weeks of twice-daily use and then use them in a pulse fashion three or four times on weekends or switch to a midpotency corticosteroid. Topical corticosteroids rarely induce a lasting remission. They may induce tachyphylaxis or cause psoriasis to become unstable. Additional measures are therefore commonly added to topical corticosteroid therapy. Calcipotriene ointment 0.005%, a vitamin D analog, is used twice daily for plaque psoriasis. Initially, patients are treated with twice-daily corticosteroids plus calcipotriene twice daily. This rapidly clears the lesions. Calcipotriene is then used alone once daily and with the corticosteroid once daily for several weeks. Eventually, the topical corticosteroids are stopped, and onceor twice-daily calcipotriene is continued long-term. Calcipotriene usually cannot be applied to the groin or on the face because of irritation. Treatment of extensive psoriasis with calcipotriene may result in hypercalcemia. Calcipotriene is incompatible with many topical corticosteroids (but not halobetasol), so if used concurrently it must be applied at a different time. Tar preparations such as Fototar cream, LCD (liquor carbonis detergens) 10% in Nutraderm lotion, alone or mixed directly with triamcinolone 0.1%, are useful adjuncts when applied twice daily. Occlusion alone has been shown to clear isolated plaques in 30–40% of patients. Occlusive hydrocolloid dressings such as thin DuoDerm are placed on the lesions and left undisturbed for as long as possible (a minimum of 5 days, up to 7 days) and then replaced. Responses may be seen within several weeks.

Tazarotene gel, a topical retinoid, is useful for the treatment of mild to moderate plaque psoriasis. About 50% of patients obtained at least 75% improvement of their skin lesions with twice-daily application, though fewer than 10% of plaques completely clear with 8 weeks of treatment. Tazarotene gel is available in 0.05% and 0.1% formulations. There is no difference between once-daily and twice-daily applications of the 0.1% formulation, but the 0.05% formulation is less effective when used once daily. Tazarotene gel appears to be similar to calcipotriene in that it may be used to augment the benefits of other forms of treatment. It is more expensive than calcipotriene and more irritating. Tazarotene gel is compatible with topical corticosteroids and may be applied simultaneously.

For the scalp, start with a tar shampoo, used daily if possible. For thick scales, use 6% salicylic acid gel (eg, Keralyt), P & S solution (phenol, mineral oil, and glycerin), or fluocinolone acetonide 0.01% in oil (DermaSmoothe/FS) under a shower cap at night, and shampoo in the morning. In order of increasing potency, triamcinolone 0.1%, or fluocinolone, betamethasone dipropionate, fluocinonide or amcinonide, and clobetasol are available in solution form for use on the scalp twice daily. Clobetasol is also available as a shampoo. For psoriasis in the body folds, treatment is difficult, since potent corticosteroids cannot be used and other agents are poorly tolerated. Tacrolimus ointment 0.1% or 0.03% or pimecrolimus cream 1% may be effective in penile, groin, and facial psoriasis.


If psoriasis involves more than 30% of the body surface, it is difficult to treat with topical agents. The treatment of choice is outpatient UVB light exposure three times weekly. Clearing occurs in an average of 7 weeks, but maintenance may be required. Severe psoriasis unresponsive to outpatient ultraviolet light may be treated in a psoriasis day care center with the Goeckerman regimen, which involves use of crude coal tar for many hours and exposure to UVB light. Such treatment may offer the best chance for prolonged remissions.

PUVA may be effective even in patients who have not responded to standard UVB treatment. Long-term use of PUVA is associated with an increased risk of skin cancer (especially squamous cell carcinoma and perhaps melanoma), particularly in persons with fair complexions. Thus, periodic examination of the skin is imperative. Atypical lentigines are a common complication. There can be rapid aging of the skin in fair individuals. Cataracts have not been reported with proper use of protective glasses. PUVA may be used in combination with other therapy, such as acitretin or methotrexate.

Parenteral corticosteroids should not be used because of the possibility of induction of pustular lesions.


Methotrexate is very effective for severe psoriasis in doses up to 25 mg once weekly. It should be used according to published protocols. Liver biopsy is performed initially after methotrexate has been used long enough by the patient to demonstrate that it is effective and well tolerated, and then at intervals depending on the cumulative dose, usually 1.5–2 g. Administration of folic acid, 1–2 mg daily, will eliminate nausea caused by methotrexate without compromising efficacy.

Acitretin, a synthetic retinoid, is most effective for pustular psoriasis in dosages of 0.5–0.75 mg/kg/d, but it also improves erythrodermic and plaque types and psoriatic arthritis. Liver enzymes and serum lipids must be checked periodically. Because acitretin is a teratogen and persists for long periods in fat, women of childbearing age must wait at least 3 years after completing acitretin treatment before considering pregnancy. When used as single agents, retinoids will flatten psoriatic plaques, but will rarely result in complete clearing. Retinoids find their greatest use when combined with phototherapy—either UVB or PUVA, with which they are synergistic.

Cyclosporine dramatically improves psoriasis and may be used to control severe cases. Rapid relapse (rebound) is the rule after cessation of therapy, so another agent must be added if cyclosporine is stopped. Systemic immunomodulators can be effective in treating psoriasis. The tumor necrosis factor (TNF) inhibitors etanercept (Enbrel), 50 mg twice weekly, and infliximab (Remicade) have shown antipsoriatic activity. Infliximab provides the most rapid response and can be used for severe pustular or erythrodermic flares. Etanercept is used more frequently for long-term treatment at a dose of 50 mg twice weekly for 3 months, then 25 mg twice weekly. Alefacept (Amevive) also improves psoriasis. Efalizumab (Raptiva), an antiCD11a monoclonal antibody has moderate efficacy. Treatment with these agents is usually effective, but in some patients the psoriasis may be worsened upon their withdrawal. High cost and potential toxicity are current limitations in the use of these new agents.


The course tends to be chronic and unpredictable, and the disease may be refractory to treatment.

Jacobi TC et al: A clinical dilemma while treating hypercholesterolaemia in psoriasis. Br J Dermatol 2003;149:1292.

Lebwohl M et al: Treatment of psoriasis. Part 1. Topical therapy and phototherapy. J Am Acad Dermatol 2001;45:487.

Lebwohl M et al: Treatment of psoriasis. Part 2. Systemic therapies. J Am Acad Dermatol 2001;45:649.

Lebwohl M et al: Psoriasis treatment: traditional therapy. Ann Rheum Dis 2005;64:ii83.

Mallbris Let al: Psoriasis phenotype at disease onset: clinical characterization of 400 adult cases. J Invest Dermatol 2005;124:499.

Mason J et al: Topical preparations for the treatment of psoriasis: a systematic review. Br J Dermatol 2002:146:351.

Yosipovitch G et al: Practical management of psoriasis in the elderly: epidemiology, clinical aspects, quality of life, patient education and treatment options. Drugs Aging 2002;19:847.



  • Oval, fawn-colored, scaly eruption following cleavage lines of trunk.

  • Herald patch precedes eruption by 1–2 weeks.

  • Occasional pruritus.

General Considerations

This is a common mild, acute inflammatory disease that is 50% more common in females. Young adults are principally affected, mostly in the spring or fall. Concurrent household cases have been reported.

Clinical Findings

Itching is common but is usually mild. The diagnosis is made by finding one or more classic lesions. The lesions consist of oval, fawn-colored plaques up to 2 cm in diameter. The centers of the lesions have a crinkled or “cigarette paper” appearance and a collarette scale, ie, a thin bit of scale that is bound at the periphery and free in the center. Only a few lesions in the eruption may have this characteristic appearance, however. Lesions follow cleavage lines on the trunk (so-called Christmas tree pattern), and the proximal portions of the extremities are often involved. A variant that affects the flexures (axillae and groin), so called inverse pityriasis rosea, and a papular variant, especially in black patients, also occur. An initial lesion (“herald patch”) that is often larger than the later lesions often precedes the general eruption by 1–2 weeks. The eruption usually lasts 6–8 weeks and heals without scarring.

Differential Diagnosis

A serologic test for syphilis should be performed if at least a few perfectly typical lesions are not present and especially if there are palmar and plantar or mucous membrane lesions or adenopathy, features that are suggestive of secondary syphilis. For the nonexpert, an RPR (rapid plasma reagin) test in all cases is not unreasonable. Tinea corporis may present with red, slightly scaly plaques, but rarely are there more than a few lesions of tinea corporis compared to the many lesions of pityriasis rosea. A scraping of scale for a KOH test will rapidly make the diagnosis. Seborrheic dermatitis on occasion presents on the body with poorly demarcated patches over the sternum, in the pubic area,


and in the axillae. The classic lesions of pityriasis rosea are not present. Tinea versicolor, viral exanthems, and drug eruptions may simulate pityriasis rosea.


Pityriasis rosea often requires no treatment. In Asians, Hispanics, or blacks, in whom lesions may remain hyperpigmented for some time, more aggressive management may be indicated. The most effective management consists of daily UVB treatments, or prednisone as used for contact dermatitis. Topical corticosteroids of medium strength (triamcinolone 0.1%) may also be used if pruritus is bothersome. Oral erythromycin for 14 days was reported to clear 73% of patients within 2 weeks (compared with none of the patients on placebo).


Pityriasis rosea is usually an acute self-limiting illness that disappears in about 6 weeks.

Karnath B et al: Pityriasis rosea. Appearance and distribution of macules aid diagnosis. Postgrad Med 2003;113:93.

Stulberg DL et al: Pityriasis rosea. Am Fam Physician 2004;69:87.



  • Dry scales and underlying erythema.

  • Scalp, central face, presternal, interscapular areas, umbilicus, and body folds.

General Considerations

Seborrheic dermatitis is an acute or chronic papulosquamous dermatitis. Seborrheic dermatitis may represent an inflammatory reaction to Malassezia yeasts.

Clinical Findings

Pruritus is an inconstant finding. The scalp, face, chest, back, umbilicus, eyelid margins, and body folds have dry scales or oily yellowish scurf. Fissuring and secondary infection are occasionally present. Patients with Parkinson's disease, patients who become acutely ill and are hospitalized, and patients with HIV infection often have seborrheic dermatitis.

Differential Diagnosis

There is a spectrum from seborrheic dermatitis to scalp psoriasis. Extensive seborrheic dermatitis may simulate intertrigo in flexural areas, but scalp, face, and sternal involvement suggests seborrheic dermatitis. Scaling of the scalp due to tinea capitis may simulate dandruff or seborrheic dermatitis, but alopecia is usually present in tinea capitis.



Shampoos that contain zinc pyrithione or selenium are used daily if possible. These may be alternated with ketoconazole shampoo (1% or 2%) used twice weekly. A combination of shampoos is used in refractory cases. Tar shampoos are also effective for milder cases and for scalp psoriasis. Topical corticosteroid solutions or lotions are then added if necessary and are used twice daily. (See treatment for scalp psoriasis, above.)


The mainstay of therapy is a mild corticosteroid (hydrocortisone 1%, alclometasone, desonide) used intermittently and not near the eyes. Potent fluorinated corticosteroids used on the face may produce steroid rosacea or atrophy and telangiectasia. These are rarely indicated for seborrheic dermatitis. If the disorder cannot be controlled with intermittent use of a topical corticosteroid alone, ketoconazole (Nizoral) 2% cream is added twice daily. Topical tacrolimus (Protopic) and pimecrolimus (Elidel) are steroid-sparing alternatives.


Low-potency corticosteroid creams—ie, 1% or 2.5% hydrocortisone, desonide, or alclometasone dipropionate—are highly effective.


Avoid greasy ointments. Apply low-potency corticosteroid lotions or creams twice daily for 5–7 days and then once or twice weekly for maintenance as necessary. Ketoconazole cream may be a useful adjunct. Tacrolimus or pimecrolimus topically may avoid corticosteroid atrophy in chronic cases.


“Marginal blepharitis” usually responds to gentle cleaning of the lid margins nightly as needed, with undiluted Johnson and Johnson Baby Shampoo using a cotton swab.


The tendency is for lifelong recurrences. Individual outbreaks may last weeks, months, or years.

Gupta AK et al: Seborrheic dermatitis. J Eur Acad Dermatol Venereol 2004;18:13.


Mycotic infections are traditionally divided into two principal groups—superficial and deep. In this chapter,


we will discuss only the superficial infections: tinea corporis and tinea cruris; dermatophytosis of the feet and dermatophytid of the hands; tinea unguium (onychomycosis); and tinea versicolor. See Chapter 36 for discussion of deep mycoses.

The diagnosis of fungal infections of the skin is usually based on the location and characteristics of the lesions and on the following laboratory examinations: (1) Direct demonstration of fungi in 10% KOH of scrapings from suspected lesions. “If it's scaly, scrape it” is a time-honored maxim. (2) Cultures of organisms from skin scrapings. (3) Histologic sections of nails stained with periodic acid-Schiff (Hotchkiss-McManus) technique may be diagnostic if scrapings and cultures are negative.

Principles of Treatment

In general, treatment follows a diagnosis confirmed by KOH preparation or culture, especially if systemic antifungal therapy is to be used. Many other diseases cause scaling, and use of an antifungal agent without a firm diagnosis makes subsequent diagnosis more difficult. In general, fungal infections are treated topically except for those involving the nails or those deep in hair follicles on the face or body.

Griseofulvin is safe and effective for treating dermatophyte infections of the skin (except for the scalp and nails). Itraconazole, an azole antifungal, accumulates in the nail plate from the matrix and nail bed and persists for 3 months after oral administration is discontinued.

Terbinafine is an allylamine oral antifungal. It has excellent activity against dermatophytes. In vitro activity against yeast forms is variable, but the drug is active against hyphal forms. It is well delivered to the nail plate and persists in the nail for 6–9 months after treatment has ended.

Fluconazole has excellent activity against yeasts and may be the treatment of choice for many forms of mucocutaneous candidiasis. Fluconazole is less effective than itraconazole or terbinafine for the treatment of dermatophytosis.

Itraconazole, fluconazole, and terbinafine can all cause elevation of liver function tests and—though rarely in the dosing regimens used for the treatment of dermatophytosis—clinical hepatitis. Ketoconazole is no longer recommended for the treatment of dermatophytosis (except for tinea versicolor) because of the higher rate of hepatitis when it is used for more than a month.

General Measures & Prevention

Since moist skin favors the growth of fungi, dry the skin carefully after bathing or after perspiring heavily. Talc or other drying powders may be useful. The use of topical corticosteroids for other diseases may be complicated by intercurrent tinea or candidal infection, and topical antifungals are often used in intertriginous areas with corticosteroids to prevent this.

1. Tinea Corporis or Tinea Circinata (Body Ringworm)


  • Ring-shaped lesions with an advancing scaly border and central clearing or scaly patches with a distinct border.

  • On exposed skin surfaces or the trunk.

  • Microscopic examination of scrapings or culture confirms the diagnosis.

General Considerations

The lesions are often on exposed areas of the body such as the face and arms. A history of exposure to an infected cat may occasionally be obtained, usually indicating microsporum infection. All species of dermatophytes may cause this disease, but Trichophyton rubrum is the most common pathogen, usually representing extension onto the trunk or extremities of tinea cruris, pedis, or manuum.

Clinical Findings


Itching may be present. In classic lesions, rings of erythema have an advancing scaly border and central clearing, occasionally with hyperpigmentation.


Hyphae can be demonstrated by removing scale and examining it microscopically using KOH. The diagnosis may be confirmed by culture.

Differential Diagnosis

Positive fungal studies distinguish tinea corporis from other skin lesions with annular configuration, such as the annular lesions of psoriasis, lupus erythematosus, syphilis, granuloma annulare, and pityriasis rosea. Psoriasis has typical lesions on elbows, knees, scalp, and nails. Secondary syphilis is often manifested by characteristic palmar, plantar, and mucous membrane lesions. Tinea corporis rarely has the large number of lesions seen in pityriasis rosea. Granuloma annulare lacks scales.


Complications include extension of the disease down the hair follicles (in which case it becomes much more difficult to cure), pyoderma, and dermatophytid.


Treat infected household pets (microsporum infections).




The following applied topically are effective against dermatophyte infections other than those of the nails: miconazole, 2% cream; clotrimazole, 1% solution, cream, or lotion; ketoconazole, 2% cream; econazole, 1% cream or lotion; sulconazole, 1% cream; oxiconazole, 1% cream; ciclopirox, 1% cream; naftifine, 1% cream or gel; butenafine cream; and terbinafine, 1% cream. Miconazole, clotrimazole, butenafine and terbinafine are available over the counter. Allylamines (especially terbinafine and butenafine) require shorter courses and lead to the most rapid response and prolonged remissions. Treatment should be continued for 1–2 weeks after clinical clearing. Betamethasone dipropionate with clotrimazole (Lotrisone) is overused by nondermatologists. In general, short-term use of betamethasone-clotrimazole does not justify the expense, and long-term improper use may result in side effects from the high-potency corticosteroid component, especially in body folds. Cases of tinea that are clinically resistant to this combination have been reported.


Griseofulvin (ultramicrosize), 250–500 mg twice daily, is used. Typically, only 4–6 weeks of therapy are required. Itraconazole as a single week-long pulse of 200 mg daily is also effective in tinea corporis. Terbinafine, 250 mg daily for 1 month, is an alternative.


Body ringworm usually responds promptly to conservative topical therapy or to griseofulvin by mouth within 4 weeks.

2. Tinea Cruris (Jock Itch)


  • Marked itching in intertriginous areas, usually sparing the scrotum.

  • Peripherally spreading, sharply demarcated, centrally clearing erythematous lesions.

  • May have associated tinea infection of feet or toenails.

  • Laboratory examination with microscope or culture confirms diagnosis.

General Considerations

Tinea cruris lesions are confined to the groin and gluteal cleft. Intractable pruritus ani may occasionally be caused by a tinea infection.

Clinical Findings


Itching may be severe, or the rash may be asymptomatic. The lesions have sharp margins, cleared centers, and active, spreading scaly peripheries. Follicular pustules are sometimes encountered. The area may be hyperpigmented on resolution.


Hyphae can be demonstrated microscopically in KOH preparations. The organism may be cultured readily.

Differential Diagnosis

Tinea cruris must be distinguished from other lesions involving the intertriginous areas, such as candidiasis, seborrheic dermatitis, intertrigo, psoriasis of body folds (“inverse psoriasis”), erythrasma, and rarely tinea versicolor. Candidiasis is generally bright red and marked by satellite papules and pustules outside of the main border of the lesion. Candida typically involves the scrotum. Tinea versicolor can be diagnosed by the KOH preparation. Seborrheic dermatitis also often involves the face, sternum, and axillae. Intertrigo tends to be more red, less scaly, and present in obese individuals in moist body folds with less extension onto the thigh. Inverse psoriasis is characterized by distinct plaques. Other areas of typical psoriatic involvement should be checked, and the KOH examination will be negative. Erythrasma is best diagnosed with Wood's light—a brilliant coral-red fluorescence is seen.



Drying powder (eg, miconazole nitrate [Zeasorb-AF]) should be dusted into the involved area in patients with excessive perspiration or occlusion of skin due to obesity. Underwear should be loose-fitting.


Any of the preparations listed in the section on tinea corporis may be used. There is great variation in expense, with miconazole, clotrimazole, butenafine, and terbinafine available over the counter and usually at a lower price. Terbinafine cream is curative in over 80% of cases after once-daily use for 7 days.


Griseofulvin ultramicrosize is reserved for severe cases. Give 250–500 mg orally twice daily for 1–2 weeks. One week of either itraconazole, 200 mg daily, or terbinafine, 250 mg daily, is also effective.


Tinea cruris usually responds promptly to topical or systemic treatment. It may leave behind postinflammatory hyperpigmentation.


3. Tinea Manuum & Tinea Pedis (Dermatophytosis, Tinea of Palms & Soles, “Athlete's Foot”)


  • Most often presenting with asymptomatic scaling.

  • May progress to fissuring or maceration in toe web spaces.

  • Itching, burning, and stinging of interdigital web; scaling palms, and soles; vesicles of soles in inflammatory cases.

  • The fungus is shown in skin scrapings examined microscopically or by culture of scrapings.

General Considerations

Tinea of the feet is an extremely common acute or chronic dermatosis. Certain individuals appear to be more susceptible than others. Most infections are caused by Trichophyton species.

Clinical Findings


The presenting symptom may be itching, burning, or stinging. Pain may indicate secondary infection with complicating cellulitis. Interdigital tinea pedis is the most common cause of leg cellulitis in healthy individuals. Tinea pedis has several presentations that vary with the location. On the sole and heel, tinea may appear as chronic noninflammatory scaling, occasionally with thickening and fissuring. This may extend over the sides of the feet in a “moccasin” distribution. The KOH preparation is usually positive. Tinea pedis often appears as a scaling or fissuring of the toe webs, perhaps with sodden maceration. As the web spaces become more macerated, the KOH preparation and fungal culture are less often positive because bacterial species begin to dominate. Finally, there may also be grouped vesicles distributed anywhere on the soles, generalized exfoliation of the skin of the soles, or nail involvement in the form of discoloration and thickening and crumbling of the nail plate.


Hyphae can be demonstrated microscopically in skin scales treated with 10% KOH. KOH and culture does not always demonstrate pathogenic fungi from macerated areas.

Differential Diagnosis

Differentiate from other skin conditions involving the same areas, such as interdigital erythrasma (use Wood's light). Psoriasis may be a cause of chronic scaling on the palms or soles and may cause nail changes. Repeated fungal cultures should be negative, and the condition will not respond to antifungal therapy. Contact dermatitis (from shoes) will often involve the dorsal surfaces and will respond to topical or systemic corticosteroids. Vesicular lesions should be differentiated from pompholyx (dyshidrosis) and scabies by proper scraping of the roofs of individual vesicles. Rarely, gram-negative organisms may cause toe web infections in the setting of prior tinea or in its absence. Culture is not very specific, because gramnegative organisms can be cultured from normal toe webs. This entity is treated with aluminum salts (see below) and imidazole antifungal agents or ciclopirox.


The essential factor in prevention is personal hygiene. Wear open-toed sandals if possible. Use of rubber or wooden sandals in community showers and bathing places is often recommended, though the effectiveness of this practice has not been studied. Careful drying between the toes after showering is essential. A hair dryer used on low setting may be used. Socks should be changed frequently, and absorbent nonsynthetic socks are preferred. Apply dusting and drying powders as necessary. The use of powders containing antifungal agents (eg, Zeasorb-AF) or chronic use of antifungal creams may prevent recurrences of tinea pedis.



  • Macerated stage—Treat with aluminum subacetate solution soaks for 20 minutes twice daily. Broadspectrum antifungal creams and solutions (containing imidazoles or ciclopirox instead of tolnaftate and haloprogin) will help combat diphtheroids and other grampositive organisms present at this stage and alone may be adequate therapy. If topical imidazoles fail, often 1 week of once-daily allylamine treatment (terbinafine or butenafine) will result in clearing.

  • Dry and scaly stage—Use any of the agents listed in the section on tinea corporis. The addition of urea 10% lotion or cream may increase the efficacy of topical treatments in thick (“moccasin”) tinea of the soles.


Griseofulvin should be used only for severe cases or those recalcitrant to topical therapy. If the infection is cleared by systemic therapy, the patient should be encouraged to begin maintenance with topical therapy, since recurrence is common. Itraconazole, 200 mg daily for 2 weeks or 400 mg daily for 1 week, or terbinafine, 250 mg daily for 2–4 weeks, may be used in refractory cases.


For many individuals, tinea pedis is a chronic affliction, temporarily cleared by therapy only to recur.


Gupta AK et al: Optimal management of fungal infections of the skin, hair, and nails. Am J Clin Dermatol 2004;5:225.

Roujeau JC et al: Chronic dermatomycoses of the foot as risk factors for acute bacterial cellulitis of the leg: a case-control study. Dermatology 2004;209:301.

Zuber TJ et al: Superficial fungal infection of the skin. Where and how it appears help determine therapy. Postgrad Med 2001;109:117, 123, 131.

4. Tinea Versicolor (Pityriasis Versicolor)


  • Velvety, tan, or pink macules or white macules that do not tan.

  • Fine scales that are not visible but are seen by scraping the lesion.

  • Central upper trunk the most frequent site.

  • Yeast and short hyphae observed on microscopic examination of scales.

General Considerations

Tinea versicolor is a mild, superficial Malassezia furfur infection of the skin (usually of the trunk). This yeast is a colonizer of all humans, which accounts for the high recurrence rate after treatment. It is not understood why some patients manifest the spore and hyphal form of the organism and the clinical disease. The eruption is often called to patients' attention by the fact that the involved areas will not tan, and the resulting hypopigmentation may be mistaken for vitiligo. A hyperpigmented form is not uncommon.

Clinical Findings


Lesions are asymptomatic, but a few patients note itching. The lesions are velvety, tan, pink, or white macules that vary from 4–5 mm in diameter to large confluent areas. The lesions initially do not look scaly, but scales may be readily obtained by scraping the area. Lesions may appear on the trunk, upper arms, neck, face, and groin.


Large, blunt hyphae and thick-walled budding spores (“spaghetti and meatballs”) may be seen when skin scales have been cleared in 10% KOH. Fungal culture is not useful.

Differential Diagnosis

Vitiligo usually presents with larger periorificial lesions. Vitiligo (and not tinea versicolor) is characterized by total depigmentation, not just a lessening of pigmentation. Vitiligo does not scale. Pink and red-brown lesions on the chest are differentiated from seborrheic dermatitis of the same areas by the KOH preparation.

Treatment & Prognosis

Topical treatments include selenium sulfide lotion, which may be applied from neck to waist daily and left on for 5–15 minutes for 7 days; this treatment is repeated weekly for a month and then monthly for maintenance. Ketoconazole shampoo, 1% or 2%, lathered on the chest and back and left on for 5 minutes may also be used weekly for maintenance. Clinicians must stress to the patient that the raised and scaly aspects of the rash are being treated; the alterations in pigmentation may take months to fade or fill in. Tinver lotion (contains sodium thiosulfate) is effective. Irritation and odor are common complaints from patients. Relapses are common.

Sulfur-salicylic acid soap or shampoo or zinc pyrithrone-containing shampoos used on a continuing basis may be effective prophylaxis.

Ketoconazole, 200 mg daily orally for 1 week or 400 mg as a single oral dose, results in short-term cure of 90% of cases. Patients should be instructed not to shower for 8–12 hours after taking ketoconazole, because it is delivered in sweat to the skin. The single dose may not work in more hot and humid areas, and more protracted therapy carries a small but finite risk of druginduced hepatitis for a completely benign disease. Without maintenance therapy, recurrences will occur in over 80% of “cured” cases over the subsequent 2 years. Treatment with a single dose of 400 mg of oral fluconazole is also effective but more expensive.

Newer imidazole creams, solutions, and lotions are quite effective for localized areas but are too expensive for use over large areas such as the chest and back.

Schwartz RA: Superficial fungal infections. Lancet 2004;364:1173.

DISCOID LUPUS ERYTHEMATOSUS (Chronic Cutaneous Lupus Erythematosus)


  • Localized red plaques, usually on the face.

  • Scaling, follicular plugging, atrophy, dyspigmentation, and telangiectasia of involved areas.

  • Histology distinctive.

  • Photosensitive.

General Considerations

Two forms of chronic cutaneous lupus erythematosus (LE) occur: chronic scarring (discoid) lesions (DLE)


and erythematous non-scarring red plaques (subacute cutaneous LE) (SCLE). Both occur most frequently in areas exposed to solar irradiation. Permanent hair loss and loss of pigmentation are common sequelae of discoid lesions. Systemic lupus erythematosus (SLE) is discussed in Chapter 20. Patients with SLE may have DLE or SCLE lesions.

Clinical Findings


Symptoms are usually mild. The lesions consist of dusky red, well-localized, single or multiple plaques, 5–20 mm in diameter, usually on the face. The scalp, external ears, and oral mucous membranes may be involved. In discoid lesions there is atrophy, telangiectasia, depigmentation, and follicular plugging. Discoid lesions may be covered by dry, horny, adherent scales. On the scalp, significant hair loss may occur.


If antinuclear antibody (ANA) is positive in high titer or when the clinical picture suggests systemic involvement, the findings of antibody to double-stranded DNA and hypocomplementemia suggest the diagnosis of SLE. Rare patients with marked photosensitivity and a picture otherwise suggestive of lupus have negative ANA tests but are positive for antibodies against Ro/SSA (SCLE). A direct immunofluorescence test reveals basement membrane antibody but may be falsely positive in sun-exposed skin.

Differential Diagnosis

The diagnosis is based on the clinical appearance confirmed by skin biopsy in all cases. In DLE, the scales are dry and “thumbtack-like” and can thus be distinguished from those of seborrheic dermatitis and psoriasis. Older lesions that have left depigmented scarring (classically in the concha of the ear) or areas of hair loss will also differentiate lupus from these diseases. Ten percent of patients with SLE have discoid skin lesions, and 5% of patients with discoid lesions have SLE. Medications (hydrochlorothiazide, calcium channel blockers) may induce chronic cutaneous LE with a positive Ro.



Protect from sunlight. Use high-SPF (> 30) sunblock with UVB and UVA coverage daily. Caution: Do not use any form of radiation therapy. Avoid using drugs that are potentially photosensitizing (eg, thiazides, piroxicam) where possible.


The following should be tried before systemic therapy: high-potency corticosteroid creams applied each night and covered with airtight, thin, pliable plastic film (eg, Saran Wrap); or Cordran tape; or ultra-high-potency corticosteroid cream or ointment applied twice daily without occlusion.


Triamcinolone acetonide suspension, 2.5–10 mg/mL, may be injected into the lesions once a month. This should be tried before systemic therapy.


1. Antimalarials

Caution: These drugs should be used only when the diagnosis is secure because they have been associated with flares of psoriasis, which may be in the differential diagnosis. They may also cause ocular changes, and ophthalmologic evaluation is required every 6 months.

a. Hydroxychloroquine sulfate

0.2–0.4 g orally daily for several months may be effective and is often used prior to chloroquine. A 3-month trial is recommended.

b. Chloroquine sulfate

250 mg daily may be effective in some cases where hydroxychloroquine is not.

c. Quinacrine (Atabrine)

100 mg daily may be the safest of the antimalarials, since eye damage has not been reported. It colors the skin yellow and is therefore not acceptable to some patients. It may be added to the above antimalarials for incomplete responses.

2. Isotretinoin

Isotretinoin, 1 mg/kg/d, is effective in chronic or subacute cutaneous LE. Recurrences are prompt and predictable on discontinuation of therapy. Because of teratogenicity, the drug is used with caution in women of childbearing age using effective contraception with negative pregnancy tests before and during therapy.

3. Thalidomide

Thalidomide is a potent teratogen but very effective in refractory cases in doses of up to 300 mg daily. Monitor for neuropathy.


The disease is persistent but not life-endangering unless systemic lupus intervenes, which is uncommon. Treatment with antimalarials is effective in perhaps 60% of cases. Although the only morbidity may be cosmetic, this can be of overwhelming significance in more darkly pigmented patients with widespread disease. Scarring alopecia can be prevented or lessened with close attention and aggressive therapy.

Patel P et al: Cutaneous lupus erythematosus: a review. Dermatol Clin 2002;20:373.



  • Localized or generalized erythematous scaling patches and plaques.

  • P.106

  • Pruritus.

  • Lymphadenopathy.

  • Distinctive histology.

General Considerations

Mycosis fungoides is a cutaneous T cell lymphoma that begins on the skin and may involve only the skin for years or decades. Certain medications (including selective serotonin reuptake inhibitors) may produce eruptions clinically and histologically identical to those of mycosis fungoides, so this possibility must always be considered.

Clinical Findings


Localized or generalized erythematous patches or plaques are present usually on the trunk. Plaques are almost always over 5 cm in diameter. Pruritus is a frequent complaint. The lesions often begin as nondescript or nondiagnostic patches, and it is not unusual for the patient to have skin lesions for more than a decade before the diagnosis can be confirmed. In more advanced cases, tumors appear. Lymphadenopathy may occur locally or widely. Lymph node enlargement may be due to benign expansion of the node (dermatopathic lymphadenopathy) or by specific involvement with mycosis fungoides.


The skin biopsy remains the basis of diagnosis, though at times numerous biopsies are required before the diagnosis can be confirmed. In addition, circulating atypical cells (S zary cells) can be detected in the blood by sensitive methods. Eosinophilia may be present.

Differential Diagnosis

Mycosis fungoides may be confused with psoriasis, a drug eruption, an eczematous dermatitis, Hansen's disease (leprosy), or tinea corporis. Histologic examination can distinguish these conditions.


The treatment of mycosis fungoides is complex. Early and aggressive treatment has not been proved to cure or prevent progression of the disease. Topical mechlorethamine ointment or solution, topical corticosteroids, UVB and PUVA are all used for early patches and plaques. Radiation therapy is effective for local lesions. Photopheresis is used at some centers. Systemic agents such as retinoids and immunomodulatory agents such as α-interferon are used alone or in various combinations for more advanced disease or in patients who fail topical therapy. Standard chemotherapeutic agents, except methotrexate, are used only when other approaches fail.


Mycosis fungoides is usually slowly progressive (over decades). Prognosis is better in patients with patch or plaque stage disease and worse in patients with erythroderma, tumors, and lymphadenopathy. Survival is not reduced in patients with limited patch disease. Elderly patients with patch and plaque stage disease commonly die of other causes. Overly aggressive treatment may lead to complications and premature demise.

Berger CL et al: Advances in understanding the immunobiology and immunotherapy of cutaneous T-cell lymphoma. Adv Dermatol 2004;20:217.

Foss F: Mycosis fungoides and the Sezary syndrome. Curr Opin Oncol 2004;16:421.

Singh F et al: Cutaneous T-cell lymphoma treatment using bexarotene and PUVA: a case series. J Am Acad Dermatol 2004;51:570.

EXFOLIATIVE DERMATITIS (Exfoliative Erythroderma)


  • Scaling and erythema over most of the body.

  • Itching, malaise, fever, chills, weight loss.

General Considerations

A preexisting dermatosis is the cause of exfoliative dermatitis in up to 63% of cases, including psoriasis, atopic dermatitis, contact dermatitis, pityriasis rubra pilaris, and seborrheic dermatitis. Reactions to topical or systemic drugs (eg, sulfonamides) account for perhaps 20–40% of cases and cancer (cutaneous T cell lymphoma, S zary syndrome) for 10–20%. Causation of the remainder is indeterminable. At the time of acute presentation, without a clear-cut prior history of skin disease or drug exposure, it may be impossible to make a specific diagnosis of the underlying condition, and diagnosis may require observation.

Clinical Findings


Symptoms may include itching, weakness, malaise, fever, and weight loss. Chills are prominent. Redness and scaling may be generalized and sometimes include loss of hair and nails. Generalized lymphadenopathy may be due to lymphoma or leukemia or may be part of the clinical picture of the skin disease (dermatopathic lymphadenitis). The mucosa is spared.



A skin biopsy is required and may show changes of a specific inflammatory dermatitis or cutaneous T cell lymphoma or leukemia. Peripheral leukocytes may show clonal rearrangements of the T cell receptor in S zary syndrome.

Differential Diagnosis

It may be impossible to identify the cause of exfoliative dermatitis early in the course of the disease, so careful follow-up is necessary. Psoriasis, severe seborrheic dermatitis, and drug eruptions may have an erythrodermic phase.


Debility (protein loss) and dehydration may develop in patients with generalized inflammatory exfoliative erythroderma; or sepsis may occur.



Home treatment is with cool to tepid baths and application of mid-potency corticosteroids under wet dressings or with the use of an occlusive plastic suit. If the exfoliative erythroderma becomes chronic and is not manageable in an outpatient setting, hospitalize the patient. Keep the room at a constant warm temperature and provide the same topical treatment as for an outpatient.


Stop all drugs, if possible. Systemic corticosteroids may provide spectacular improvement in severe or fulminant exfoliative dermatitis, but long-term therapy should be avoided (see Chapter 26). In addition, systemic corticosteroids must be used with caution because some patients with erythroderma have psoriasis and could develop pustular psoriasis. For cases of psoriatic erythroderma and pityriasis rubra pilaris, either acitretin or methotrexate may be indicated. Erythroderma secondary to lymphoma or leukemia requires specific topical or systemic chemotherapy. Suitable antibiotic drugs with coverage for staphylococcus should be given when there is evidence of bacterial infection.


Most patients recover completely or improve greatly over time but may require long-term therapy. Deaths are rare in the absence of cutaneous T cell lymphoma. A minority of patients will suffer from undiminished erythroderma for indefinite periods.

Balasubramaniam P et al: Erythroderma: 90% skin failure. Hosp Med 2004;65:100.

Gallelli L et al: Generalized exfoliative dermatitis induced by interferon alfa. Ann Pharmacother 2004;38:2173.

Jaffer AN et al: Exfoliative dermatitis. Erythroderma can be a sign of a significant underlying disorder. Postgrad Med 2005;117:49.

Shegal VN et al: Erythroderma/exfoliative dermatitis: a synopsis. Int J Dermatol 2004;43:39.


Isolated scaly patches may represent actinic (solar) keratoses, nonpigmented seborrheic keratoses, or Bowen's or Paget's disease.

Actinic Keratoses

Actinic keratoses are small (0.2–0.6 cm) patches—fleshcolored, pink, or slightly hyperpigmented—that feel like sandpaper and are tender when the finger is drawn over them. They occur on sun-exposed parts of the body in persons of fair complexion. Actinic keratoses are considered premalignant, but only 1:1000 lesions per year progress to become squamous cell carcinomas.

Application of liquid nitrogen is a rapid and effective method of eradication. The lesions crust and disappear in 10–14 days. An alternative treatment is the use of fluorouracil cream. This agent may be rubbed into the lesions morning and night until they become first red and sore and then crusted and eroded (usually 2–3 weeks), and then stopped. Carac (0.5% fluorouracil) may be used once daily for a longer period (4 weeks to several months). Keratoses may clear with less irritation. Imiquimod 5% cream applied two to three times weekly for 3–6 weeks is the more costly alternative to topical fluorouracil (5FU). Any lesions that persist should be evaluated for possible biopsy.

Jorizzo JL: Current and novel treatment options for actinic keratoses. J Cutan Med Surg 2004;8 Suppl 3:13.

Silapunt S et al: Topical and light-based treatments for actinic keratoses. Semin Cutan Med Surg 2003;22:162.

Weiss J et al: Effective treatment of actinic keratosis with 0.5% fluorouracil cream for 1, 2, or 4 weeks. Cutis 2002:70(2 Suppl):22.

Bowen's Disease & Paget's Disease

Bowen's disease (intraepidermal squamous cell carcinoma) occurs either on sun-exposed or sun-protected cutaneous surfaces. The lesion is usually a small (1–3 cm), well-demarcated, slightly raised, pink to red, scaly plaque and may resemble psoriasis or a large actinic keratosis. While it may take some time, these lesions may progress to invasive squamous cell carcinoma. Excision or other definitive treatment is indicated.

Extramammary Paget's disease, a manifestation of apocrine sweat gland carcinoma or underlying genitourinary or gastrointestinal cancer, resembles chronic eczema and usually involves apocrine areas such as the genitalia. Mammary Paget's disease of the nipple, a unilateral or rarely bilateral red scaling plaque that


may ooze, is associated with an underlying intraductal mammary carcinoma.

Nishimura Y et al: Bilateral Bowen's disease. Br J Dermatol 2004;151:227.

Shepherd V et al: Extramammary Paget's disease. BJOG 2005;112:273.


Intertrigo is caused by the macerating effect of heat, moisture, and friction. It is especially likely to occur in obese persons and in humid climates. The symptoms are itching, stinging, and burning. The body folds develop fissures, erythema, and sodden epidermis, with superficial denudation. Candidiasis may complicate intertrigo. “Inverse psoriasis,” tinea cruris, erythrasma, and candidiasis must be ruled out.

Maintain hygiene in the area, and keep it dry. Compresses may be useful acutely. Hydrocortisone 1% and an imidazole cream or nystatin cream are effective. Recurrences are common.


HERPES SIMPLEX (Cold or Fever Sore; Genital Herpes)


  • Recurrent small grouped vesicles on an erythematous base, especially in the orolabial and genital areas.

  • May follow minor infections, trauma, stress, or sun exposure; regional lymph nodes may be swollen and tender.

  • Tzanck smear is positive for multinucleated epithelial giant cells; viral cultures and direct fluorescent antibody tests are positive.

General Considerations

Over 85% of adults have serologic evidence of herpes simplex type 1 (HSV-1) infections, most often acquired asymptomatically in childhood. Occasionally, primary infections may be manifested as severe gingivostomatitis. Thereafter, the patient may have recurrent self-limited attacks, provoked by sun exposure, orofacial surgery, fever, or a viral infection.

About 25% of the United States population has serologic evidence of infection with herpes simplex type 2 (HSV-2). HSV-2 causes lesions whose morphology and natural history are similar to those caused by HSV-1 on the genitalia of both sexes. The infection is acquired by sexual contact. In monogamous heterosexual couples where one partner has HSV-2 infection, seroconversion of the noninfected partner occurs in 10% over a 1-year period. Up to 70% of such infections appeared to be transmitted during periods of asymptomatic shedding. Owing to changes in sexual behavior, up to 40% of newly acquired cases of genital herpes are due to HSV-1.

Clinical Findings


The principal symptoms are burning and stinging. Neuralgia may precede or accompany attacks. The lesions consist of small, grouped vesicles that can occur anywhere but which most often occur on the vermilion border of the lips, the penile shaft, the labia, the perianal skin, and the buttocks. Regional lymph nodes may be swollen and tender. The lesions usually crust and heal in 1 week. Patients can be educated to recognize attacks that they previously did not identify as recurrent herpes simplex. Herpes simplex is the most common cause of painful genital ulcerations in patients with HIV infection.


Lesions of herpes simplex must be distinguished from chancroid, syphilis, pyoderma, or trauma. Direct immunofluorescent antibody slide tests offer rapid, sensitive diagnosis. Viral culture may also be helpful. The Tzanck smear, which demonstrates multinucleated cells, is the least sensitive test. Herpes simplex and varicella-zoster viruses cannot be distinguished on the Tzanck smear. Herpes serology is not used in the diagnosis of an acute genital ulcer. However, specific HSV-2 serology by Western blot assay or enzyme-linked immunosorbent assay (ELISA) can determine who is HSV-infected and potentially infectious. Such testing is very useful in couples in which only one partner reports a history of genital herpes.


Complications include pyoderma, eczema herpeticum, herpetic whitlow, herpes gladiatorum (epidemic herpes in wrestlers transmitted by contact), esophagitis, neonatal infection, keratitis, and encephalitis.


Sunscreens are useful adjuncts in preventing sun-induced recurrences. Prophylactic use of oral acyclovir may prevent recurrences. Acyclovir should be started at a dosage of 200 mg four times daily beginning 24 hours prior to ultraviolet light exposure, dental surgery, or orolabial cosmetic surgery. Comparable doses are 500 mg twice daily for valacyclovir and 250 mg twice daily for famciclovir.



Three systemic agents are available for the treatment of herpes infections: acyclovir, its valine analog valacyclovir,


and famciclovir. All three agents are very effective and, when used properly, virtually nontoxic. Only acyclovir is available for intravenous administration. In the immunocompetent, with the exception of severe orolabial herpes, only genital disease is treated. For first clinical episodes of herpes simplex, the dosage of acyclovir is 200 mg orally five times daily (or 800 mg three times daily); of valacyclovir, 1000 mg twice daily; and of famciclovir, 250 mg three times daily. The duration of treatment is from 7 to 10 days depending on the severity of the outbreak. Most cases of recurrent herpes are mild and do not require therapy. In addition, pharmacotherapy of recurrent HSV is of limited benefit, with studies finding a reduction in the average outbreak by only 12–24 hours. If treatment is desired, recurrent genital herpes outbreaks may be treated with 3 days of valacyclovir, 500 mg twice daily, or with 5 days of acyclovir, 200 mg five times a day; or famciclovir, 125 mg twice daily. Valacyclovir, 2 g twice daily for 1 day, is approved for recurrences of orolabial herpes. The addition of a potent topical corticosteroid three times daily reduces the duration, size, and pain of orolabial herpes treated with an oral antiviral agent.

In patients with frequent or severe recurrences, suppressive therapy is most effective in controlling disease. Suppressive treatment will reduce outbreaks by 85% and reduces viral shedding by more than 90%. This results in about a 50% reduced risk of transmissions. The recommended suppressive doses, taken continuously, are acyclovir, 400 mg twice daily; valacyclovir, 500 mg once daily; or famciclovir, 125–250 mg twice daily. Long-term suppression appears very safe, and after 5–7 years a substantial proportion of patients can discontinue treatment. The use of condoms, patient education, and long-term suppressive oral antiviral therapy are all effective in reducing transmission of genital herpes. However, there is nothing—alone or in combination—that absolutely prevents transmission.


In general, topical therapy is not effective. It is strongly urged that 5% acyclovir ointment, if used at all, be limited to the restricted indications for which it has been approved, ie, initial herpes genitalis and mucocutaneous herpes simplex infections in immunocompromised patients. Penciclovir cream, to be applied at the first symptom every 2 hours while awake for 4 days for recurrent orolabial herpes, reduces the average attack duration from 5 days to 4.5 days.


Aside from the complications described above, recurrent attacks last several days, and patients recover without sequelae.

Corey L et al: Once-daily valacyclovir to reduce the risk of transmission of genital herpes. N Engl J Med 2004;350:67.

Spruance SL et al: Combination treatment with famciclovir and a topical corticosteroid gel versus famciclovir alone for experimental ultraviolet radiation-induced herpes simplex labialis: a pilot study. J Infect Dis 2000;181:1906.



  • Pain along the course of a nerve followed by grouped vesicular lesions.

  • Involvement is unilateral; some lesions (< 20) may occur outside the affected dermatome.

  • Lesions are usually on face or trunk.

  • Direct fluorescent antibody positive, especially in vesicular lesions.

General Considerations

Herpes zoster is an acute vesicular eruption due to the varicella-zoster virus. It usually occurs in adults. With rare exceptions, patients suffer only one attack. Dermatomal herpes zoster does not imply the presence of a visceral malignancy. Generalized disease, however, raises the suspicion of an associated immunosuppressive disorder such as Hodgkin's disease or HIV infection. HIV-infected patients are 20 times more likely to develop zoster, often before other clinical findings of HIV disease are present. A history of HIV risk factors and HIV testing when appropriate should be considered, especially in patients with zoster who are younger than 55 years.

Clinical Findings

Pain usually precedes the eruption by 48 hours or more and may persist and actually increase in intensity after the lesions have disappeared. The lesions consist of grouped, tense, deep-seated vesicles distributed unilaterally along a dermatome. The most common distributions are on the trunk or face. Up to 20 lesions may be found outside the affected dermatomes. Regional lymph glands may be tender and swollen.

Differential Diagnosis

Since poison oak and poison ivy dermatitis can occur unilaterally, they must be differentiated at times from herpes zoster. Allergic contact dermatitis is pruritic; zoster is painful. One must differentiate herpes zoster from lesions of herpes simplex, which occasionally occurs in a dermatomal distribution. Doses of antivirals appropriate for zoster should be used in the absence of a clear diagnosis. Facial zoster may simulate erysipelas initially, but zoster is unilateral and shows vesicles after 24–48 hours. The pain of preeruptive herpes zoster


may lead the clinician to diagnose migraine, myocardial infarction, acute abdomen, herniated nucleus pulposus, etc, depending on the dermatome involved.


Sacral zoster may be associated with bladder and bowel dysfunction. Persistent neuralgia, anesthesia or scarring of the affected area following healing, facial or other nerve paralysis, and encephalitis may occur. Postherpetic neuralgia is most common after involvement of the trigeminal region, and in patients over the age of 55. Early (within 72 hours after onset) and aggressive antiviral treatment of herpes zoster reduces the severity and duration of postherpetic neuralgia. Zoster ophthalmicus (V1) can result in visual impairment.



1. Immunocompetent host

Since early treatment of zoster reduces postherpetic neuralgia, those with a risk of developing this complication should be treated, ie, those over age 55. In addition, younger patients with acute moderate to severe pain may benefit from effective antiviral therapy. Treatment can be given with oral acyclovir, 800 mg five times daily; famciclovir, 500 mg three times daily; or valacyclovir, 1 g three times daily—all for 7 days (see Chapter 37). For reasons of increased bioavailability and ease of dosing schedule, the preferred agents are those given three times daily. Patients should maintain good hydration. The dose of antiviral should be adjusted for renal function as recommended. Nerve blocks may be important in the management of initial severe pain. Ophthalmologic consultation is vital for involvement of the first branch of the trigeminal nerve. Systemic corticosteroids are effective in reducing acute pain, improving quality of life, and returning patients to normal activities much more quickly. They do not increase the risk of dissemination in immunocompetent hosts. If not contraindicated, a tapering 3-week course of prednisone, starting at 60 mg/d, should be considered for its adjunctive benefit in immunocompetent patients. Oral corticosteroids do not reduce the prevalence, severity, or duration of postherpetic neuralgia beyond that achieved by effective antiviral therapy.

2. Immunocompromised host

Given the safety and efficacy of currently available antivirals, most immunocompromised patients with herpes zoster are candidates for antiviral therapy. The dosage schedule is as listed above, but treatment should be continued until the lesions have completely crusted and are healed or almost healed (up to 2 weeks). Because corticosteroids increase the risk of dissemination, they should not be given adjunctively in immunosuppressed patients. Progression of disease may necessitate intravenous therapy with acyclovir, 10 mg/kg intravenously, three times daily. After 3–4 days, oral therapy may be substituted if there has been a good response to intravenous therapy. Adverse effects include decreased renal function from crystallization, nausea and vomiting, and abdominal pain.

Foscarnet, administered in a dosage of 40 mg/kg two or three times daily intravenously, is indicated for treatment of acyclovir-resistant varicella-zoster virus infections.


Calamine or starch shake lotions may be of some help.


The most effective treatment is prevention with early and aggressive antiviral therapy. Once established, postherpetic neuralgia may be treated with capsaicin ointment, 0.025–0.075%, or lidocaine (Lidoderm) topical patches. Chronic postherpetic neuralgia may be relieved by regional blocks (stellate ganglion, epidural, local infiltration, or peripheral nerve), with or without corticosteroids added to the injections. Amitriptyline, 25–75 mg as a single nightly dose, is the first-line oral therapy beyond simple analgesics. Gabapentin, up to 3600 mg daily (starting at 300 mg three times daily), may be added for additional pain relief.


The eruption persists 2–3 weeks and usually does not recur. Motor involvement in 2–3% of patients may lead to temporary palsy.

Vanhems P et al: The incidence of herpes zoster is less likely than other opportunistic infections to be reduced by highly active antiretroviral therapy. J Acquir Immune Defic Syndr 2005; 38:111.

Wareham D: Postherpetic neuralgia. Clin Evid 2003;10:942.

Wassilew S; Collaborative Brivudin PHN Study Group: Brivudin compared with famciclovir in the treatment of herpes zoster: effects in acute disease and chronic pain in immunocompetent patients. A randomized, double-blind, multinational study. J Eur Acad Dermatol Venereol 2005;19:47.



  • Prodromal high fever.

  • Eruption progressing from papules to vesicles to pustules, then crusts.

  • All lesions in the same stage.

  • Face and distal extremities (including palms and soles) favored.


General Considerations

Concern for the use of smallpox virus as a bioterrorist weapon has led to the reintroduction of vaccination in some segments of the population (first responders and the military).

Clinical Findings

The incubation period for variola averages 12 days (7–17 days). The prodrome begins with abrupt onset of high fever, severe headaches, and backaches. At this stage, the infected person appears quite ill. The infectious phase begins with the appearance of an enanthem, followed in 1–2 days by a skin eruption. The lesions begin as macules, progressing to papules, then pustules, and finally crusts over 14–18 days. The face and distal extremities are favored. The face is affected first, followed by the upper extremities, then the lower extremities and trunk, completely evolving over 1 week. Lesions are relatively monomorphous, especially in each anatomic region.

Inculation with vaccinia produces a papular lesion on day 2–3 that progresses to an umbilicated papule by day 4 and a pustular lesion by the end of the first week. The lesion then collapses centrally, and crusts. The crust eventually detaches up to a month after the inoculation. Persons with eczema should not be immunized as they may suffer widespread vaccinia (eczema vaccinatum) whose lesions might resemble those of smallpox. Vaccinia is moderately contagious, and patients with atopic dermatitis and Darier's disease may acquire severe generalized disease by exposure to a recently vaccinated person. Generalized vaccinia may be fatal. Prior vaccination does not prevent generalized vaccinia, but previously vaccinated individuals have milder disease. Progressive vaccinia (vaccinia gangrenosum)—progression of the primary inoculation site to a large ulceration—occurs in persons with systemic immune deficiency. It can have a fatal outcome.

Differential Diagnosis

Smallpox and vaccinia are to be distinguished from generalized varicella zoster virus infection or generalized herpes simplex. The latter two viral infections are not associated with a severe febrile prodrome. Lesions are at various stages at each anatomic site. Varicella usually appears in waves or crops. Multiple palm and sole lesions are common in variola and uncommon in generalized varicella-zoster and herpes simplex infection.

Direct fluorescent antibody testing for HSV and varicella zoster virus are the first-line diagnostic tests to differentiate varicella zoster virus, HSV, vaccinia, and variola. Until the diagnosis is confirmed, strict isolation of the patient is indicated. Similar fluorescent testing for variola can be performed in special laboratories.


There is no specific and proven antiviral therapy for vaccinia or variola. Vaccinia immune globulin is used to treat eczema vaccinatum and progressive vaccinia. Cidofovir may have some activity against these poxviruses.

Breman J et al: Diagnosis and management of smallpox. N Engl J Med 2002;346:1300.

Sepkowitz K: How contagious is vaccinia? N Engl J Med 2003;348:439.



  • “Tapioca” vesicles of 1–2 mm on the palms, soles, and sides of fingers, associated with pruritus.

  • Vesicles may coalesce to form multiloculated blisters.

  • Scaling and fissuring may follow drying of the blisters.

  • Appearance in the third decade, with lifelong recurrences.

General Considerations

“Dyshidrotic eczema” is a misnomer, suggesting that the vesicles of this condition are related to eccrine sweat ducts and sweating, which they are not. This is an extremely common form of hand dermatitis, preferably called pompholyx (Gr “bubble”) or vesiculobullous dermatitis of the palms and soles. Patients often have an atopic background and report flares with stress. Patients with widespread dermatitis due to any cause may develop pompholyx-like eruptions as a part of an autoeczematization response.

Clinical Findings

Small clear vesicles stud the skin at the sides of the fingers and on the palms or soles. They look like the grains in tapioca. They may be associated with intense itching. Later, the vesicles dry and the area becomes scaly and fissured.

Differential Diagnosis

Unroofing the vesicles and examining the blister roof with a KOH preparation will reveal hyphae in cases of bullous tinea. Blisters extending onto the dorsum of the hands may represent allergic contact dermatitis, and the culprit must be sought by history or by patch testing. Patients with inflammatory tinea pedis may have a vesicular dermatophytid of the palms. Always examine the feet of a patient with a hand eruption. Nonsteroidal anti-inflammatory drugs (NSAIDs) may


produce an eruption very similar to that of dyshidrosis on the hands.


There is no known way to prevent attacks.


Topical and systemic corticosteroids help some patients dramatically. Since this is a chronic problem, systemic corticosteroids are generally not appropriate therapy. A high-potency topical corticosteroid used early in the attack may help abort the flare and ameliorate pruritus. Topical corticosteroids are also important in treating the scaling and fissuring that are seen after the vesicular phase. It is essential that patients avoid anything that irritates the skin; they should wear cotton gloves inside vinyl gloves when doing dishes or other wet chores, use long-handled brushes instead of sponges, and use a hand cream after washing the hands. Patients respond to PUVA therapy and injection of botulinum toxin into the palms as for hyperhidrosis.


For most patients, the disease is an inconvenience. For some, vesiculobullous hand eczema can be incapacitating.

Swartling C et al: Treatment of dyshidrotic hand dermatitis with intradermal botulinum toxin. J Am Acad Dermatol 2002: 47:667.



  • Noninflammatory blisters on sun-exposed sites, especially the dorsal surfaces of the hands.

  • Hypertrichosis, skin fragility.

  • Associated liver disease.

  • Elevated urine porphyrins.

General Considerations

Porphyria cutanea tarda is the most common type of porphyria. Cases are sporadic or hereditary. The disease is associated with ingestion of certain medications (eg, estrogens), and liver disease from alcoholism or hepatitis C. In patients with liver disease, hemosiderosis is often present.

Clinical Findings


Patients complain of painless blistering and fragility of the skin of the dorsal surfaces of the hands. Facial hypertrichosis and hyperpigmentation are common.


Urinary uroporphyrins are elevated twofold to fivefold above coproporphyrins. Patients may also have abnormal liver function tests, evidence of hepatitis C infection, increased liver iron stores, and hemochromatosis gene mutations. Multiple triggering factors are often discovered.

Differential Diagnosis

Skin lesions identical to those of porphyria cutanea tarda may be seen in patients who receive maintenance dialysis and in those who take certain medications (tetracyclines and NSAIDs, especially naproxen). In this so-called pseudoporphyria, the biopsy results are identical to those associated with porphyria cutanea tarda, but urine porphyrins are normal.


Although the lesions are triggered by sun exposure, the wavelength of light triggering the lesions is beyond that absorbed by sunscreens, which for that reason are ineffective. Barrier sun protection with clothing is required.


Stopping all triggering medications and substantially reducing or stopping alcohol consumption may alone lead to improvement. Phlebotomy without oral iron supplementation at a rate of 1 unit every 2–4 weeks will gradually lead to improvement. Very low dose antimalarials (as low as 200 mg of hydroxychloroquine twice weekly), alone or in combination with phlebotomy, will increase the excretion of porphyrins, improving the skin disease. Treatment is continued until the patient is asymptomatic. Urine porphyrins may be monitored.


Most patients improve with treatment. Sclerodermoid skin lesions may develop on the trunk, scalp, and face.

Aziz Ibrahim A et al: Porphyria cutanea tarda in pregnancy: a case report. J Obstet Gynaecol 2004;24:574.

Dolan CK et al: Pseudoporphyria as a result of voriconazole use: a case report. Int J Dermatol 2004;43:768.

Hsu S: Skin fragility of the hands. Am Fam Physician 2004;15: 753.

Mehrany K et al: Association of porphyria cutanea tarda with hereditary hemochromatosis. J Am Acad Dermatol 2004;51: 205.

Phung TL et al: Beta-lactam antibiotic-induced pseudoporphyria. J Am Acad Dermatol 2004;51(2 Suppl):S80.


Dermatitis herpetiformis is an uncommon disease manifested by pruritic papules, vesicles, and papulovesicles mainly on the elbows, knees, buttocks, posterior neck, and scalp. It appears to have its highest prevalence in Scandinavia and is associated with HLA antigens -B8,


-DR3, and -DQ2. The diagnosis is made by light microscopy, which demonstrates neutrophils at the dermal papillary tips. Direct immunofluorescence studies show granular deposits of IgA in the dermal papillae. Circulating antiendomysium antibodies and antibodies to tissue transglutaminase are present in 70% of cases. Patients have gluten-sensitive enteropathy, but for the great majority it is subclinical. However, ingestion of gluten is the cause of the disease, and strict long-term avoidance of dietary gluten has been shown to decrease the dose of dapsone (usually 100–200 mg/d) required to control the disease and may even eliminate the need for drug treatment. Although adherence to a gluten-free diet is difficult, the availability of many gluten-free foods makes this easier to accomplish. Patients with dermatitis herpetiformis are at increased risk for development of gastrointestinal lymphoma, and this risk is reduced by a gluten-free diet.

Borghi-Scoazec G et al: Onset of dermatitis herpetiformis after treatment by interferon and ribavirin for chronic hepatitis C. J Hepatol 2004;40:871.

Stroubou E et al: Ursodeoxycholic acid causing exacerbation of dermatitis herpetiformis. J Am Acad Dermatol 2001;45:319.

Zone JJ et al: Warning: Bread may be harmful to your health. J Am Acad Dermatol 2004;51:27.




  • Superficial blisters filled with purulent material that rupture easily.

  • Crusted superficial erosions.

  • Positive Gram stain and bacterial culture.

General Considerations

Impetigo is a contagious and autoinoculable infection of the skin caused by staphylococci or streptococci (or both). Classically, two forms have been recognized: (1) a vesiculopustular type, with thick golden-crusted lesions caused by S aureus or group A β-hemolytic streptococci; and (2) a bullous type, associated with phage group II S aureus. However, most cases of impetigo of either presentation now appear to be due to staphylococci.

Clinical Findings


Itching is the only symptom. The lesions consist of macules, vesicles, bullae, pustules, and honey-colored gummy crusts that when removed leave denuded red areas. The face and other exposed parts are most often involved. Ecthyma is a deeper form of impetigo caused by staphylococci or streptococci, with ulceration and scarring. It occurs frequently on the extremities.


Gram stain and culture confirm the diagnosis.

Differential Diagnosis

The main differential diagnoses are acute allergic contact dermatitis and herpes simplex. Contact dermatitis may be suggested by the history or by linear distribution of the lesions, and culture should be negative for staphylococci and streptococci. Herpes simplex infection usually presents with grouped vesicles or discrete erosions and may be associated with a history of recurrences. Viral cultures are positive.


Topical antibiotics are not as effective as systemic antibiotics. In most cases, systemic antibiotics are indicated. Cephalexin, 250 mg four times daily, is usually effective. Doxycycline, 100 mg twice daily, is a reasonable alternative. Community-acquired methicillin-resistant S aureus (CA-MRSA) may cause impetigo, and initial coverage for MRSA could include doxycycline, clindamycin, or trimethoprim-sulfamethoxazole.Quinolones have poor activity against streptococci. About 50% of CA-MRSA are quinolone resistant. Recurrent impetigo is associated with nasal carriage of S aureus, treated with rifampin, 600 mg daily, or intranasal mupirocin ointment twice daily for 5 days.

Crusts and weepy areas may be treated with compresses, and washcloths and towels must be segregated and washed separately.

Hirschmann JV: Impetigo: etiology and therapy. Curr Clin Top Infect Dis 2002:22:42.

Levine N: Eruption on the face. Bulla formation and crusting on the forehead and nose can be easily treated. Geriatrics 2002;57:17.



  • Erythema and edema, with pruritus, often followed by vesicles and bullae in an area of contact with a suspected agent.

  • Later, weeping, crusting, or secondary infection.

  • A history of previous reaction to suspected contactant.

  • Patch test with agent positive.


General Considerations

Contact dermatitis is an acute or chronic dermatitis that results from direct skin contact with chemicals or allergens. Eighty percent of cases are due to excessive exposure to or additive effects of primary or universal irritants (eg, soaps, detergents, organic solvents) and are called irritant contact dermatitis. The minority are due to actual contact allergy such as poison ivy or poison oak. The most common topicals causing allergic rashes include antimicrobials (especially bacitracin and neomycin), antihistamines, anesthetics (benzocaine), hair dyes, preservatives (eg, parabens), jewelry (nickel), latex, vitamin E, essential oils, and adhesive tape. Occupational exposure is an important cause of allergic contact dermatitis. Weeping and crusting are typically due to allergic and not irritant dermatitis, which often appears red and scaly. Contact dermatitis due to latex rubber in gloves is of special concern in health care workers.

Clinical Findings


In allergic contact dermatitis, the acute phase is characterized by tiny vesicles and weepy and crusted lesions, whereas resolving or chronic contact dermatitis presents with scaling, erythema, and possibly thickened skin. Itching, burning, and stinging may be severe. The lesions, distributed on exposed parts or in bizarre asymmetric patterns, consist of erythematous macules, papules, and vesicles. The affected area is often hot and swollen, with exudation and crusting, simulating—and at times complicated by—infection. The pattern of the eruption may be diagnostic (eg, typical linear streaked vesicles on the extremities in poison oak or ivy dermatitis). The location will often suggest the cause: Scalp involvement suggests hair tints, sprays, or tonics; face involvement, creams, cosmetics, soaps, shaving materials, nail polish; and neck involvement, jewelry, hair dyes, etc.


Gram stain and culture will rule out impetigo or secondary infection (impetiginization). If itching is generalized and impetiginized scabies is considered, a scraping for mites should be done. After the episode has cleared, the patch test may be useful if the triggering allergen is not known. In suspected photocontact dermatitis—involvement of face, “V” (suprasternal notch) of the upper chest, and hands, sparing the skin under the nose, chin, and inner upper eyelid—photopatch tests may be done by exposing the traditional patch test site to ultraviolet light after 24 hours.

Differential Diagnosis

Asymmetric distribution, blotchy erythema around the face, linear lesions, and a history of exposure help distinguish acute contact dermatitis from other skin lesions. The most commonly mistaken diagnosis is impetigo. Chronic allergic contact dermatitis must be differentiated from scabies, dermatophytid, atopic dermatitis, pompholyx, and other eczemas.


Prompt and thorough removal of allergens by washing with water or solvents or other chemical agents may be effective if done very shortly after exposure to poison oak or ivy. Several over-the-counter barrier creams (eg, Stokogard, Ivy Shield) offer some protection to patients at high risk for poison oak and ivy dermatitis if applied before exposure. Iodoquinol cream may benefit nickel allergic patients in a similar manner. Ingestion of rhus antigen is of limited clinical value for the induction of tolerance.

The mainstay of prevention is identification of agents causing the dermatitis and avoidance of exposure or use of protective clothing and gloves. In industry-related cases, prevention may be accomplished by moving or retraining the worker.



While local measures are important, severe or widespread involvement is difficult to manage without systemic corticosteroids because even the highest-potency topical corticosteroids seem not to work well on vesicular and weepy lesions. Localized involvement (except on the face) can often be managed solely with topical agents. Irritant contact dermatitis is treated by protection from the irritant and use of topical corticosteroids as for atopic dermatitis (described above). The treatment of allergic contact dermatitis is detailed below.


1. Acute weeping dermatitis

Compresses are most often used. It is unwise to scrub lesions with soap and water. Calamine or starch shake lotions may sometimes be used in intervals between wet dressings, especially for involvement of intertriginous areas or when oozing is not marked. Lesions on the extremities may be bandaged with wet dressings for 30–60 minutes several times a day. Potent topical corticosteroids in gel or cream form may help suppress acute contact dermatitis and relieve itching. In cases where weeping is marked or in intertriginous areas, ointments will make the skin even more macerated and should be avoided. Suggested preparations are fluocinonide gel, 0.05%, used two or three times daily with compresses, or clobetasol or halobetasol cream, used twice daily for a maximum of 2 weeks—not in body folds or on the face. This should be followed by tapering of the number of applications per day or use of a mid-potency corticosteroid such as triamcinolone 0.1% cream to prevent rebound of the dermatitis. A soothing formulation is 2 oz of 0.1% triamcinolone acetonide cream in 7.5 oz Sarna lotion (0.5% camphor, 0.5% menthol, 0.5% phenol) mixed by the patient.


2. Subacute dermatitis (subsiding)

Mid-potency (triamcinolone 0.1%) to high-potency corticosteroids (amcinonide, fluocinonide, desoximetasone) are the mainstays of therapy.

3. Chronic dermatitis (dry and lichenified)

Highto highest-potency corticosteroids are used in ointment form.


For acute severe cases, prednisone may be given orally for 12–21 days. Prednisone, 60 mg for 4–7 days, 40 mg for 4–7 days, and 20 mg for 4–7 days without a further taper is one useful regimen. Another is to dispense seventy-eight 5-mg pills to be taken 12 the first day, 11 the second day, and so on. The key is to use enough corticosteroid (and as early as possible) to achieve a clinical effect and to taper slowly enough to avoid rebound. A Medrol Dosepak (methylprednisolone) with 5 days of medication is inappropriate on both counts. (See Chapter 26.)


Allergic contact dermatitis is self-limited if reexposure is prevented but often takes 2–3 weeks for full resolution.

Arbogast JW et al: Effectiveness of a hand care regimen with moisturizer in manufacturing facilities where workers are prone to occupation irritant dermatitis. Dermatitis 2004;15:10.

Goodall J: Oral corticosteroids for poison ivy dermatitis. CMAJ 2002;166:300.

Kist JM et al: The contact allergen replacement database and treatment of allergic contact dermatitis. Arch Dermatol 2004;140:1448.




  • Occurs at puberty, though onset may be delayed into the third or fourth decade.

  • Open and closed comedones are the hallmark of acne vulgaris.

  • The most common of all skin conditions.

  • Severity varies from purely comedonal to papular or pustular inflammatory acne to cysts or nodules.

  • Face and trunk may be affected.

  • Scarring may be a sequela of the disease or picking and manipulating by the patient.

General Considerations

Acne vulgaris is polymorphic. Open and closed comedones, papules, pustules, and cysts are found. The disease is activated by androgens in those who are genetically predisposed.

Acne vulgaris is more common and more severe in males. It does not always clear spontaneously when maturity is reached. Twelve percent of women and 3% of men over age 25 have acne vulgaris. This rate does not decrease until after age 44. The skin lesions parallel sebaceous activity. Pathogenic events include plugging of the infundibulum of the follicles, retention of sebum, overgrowth of the acne bacillus (Propionibacterium acnes) with resultant release of and irritation by accumulated fatty acids, and foreign body reaction to extrafollicular sebum. The mechanism of antibiotics in controlling acne is not clearly understood, but they may work because of their antibacterial or anti-inflammatory properties.

When a resistant case of acne is encountered in a woman, hyperandrogenism may be suspected. This may or may not be accompanied by hirsutism, irregular menses, or other signs of virilism.

Clinical Findings

There may be mild soreness, pain, or itching. The lesions occur mainly over the face, neck, upper chest, back, and shoulders. Comedones are the hallmark of acne vulgaris. Closed comedones are tiny, flesh-colored, noninflamed bumps that give the skin a rough texture or appearance. Open comedones typically are a bit larger and have black material in them. Inflammatory papules, pustules, ectatic pores, acne cysts, and scarring are also seen.

Acne may have different presentations at different ages. Preteens often present with comedones as their first lesions. Inflammatory lesions in young teenagers are often found in the middle of the face, extending outward as the patient becomes older. Women in their third and fourth decades (often with no prior history of acne) commonly present with papular lesions on the chin and around the mouth—so-called perioral dermatitis.

Differential Diagnosis

In adults, acne rosacea presents with papules and pustules in the middle third of the face, but telangiectasia, flushing, and the absence of comedones distinguish this disease from acne vulgaris. A pustular eruption on the face in patients receiving antibiotics or with otitis externa should be investigated with culture to rule out an uncommon gram-negative folliculitis. Acne may develop in patients who use systemic corticosteroids or topical fluorinated corticosteroids on the face. Acne may be exacerbated or caused by irritating creams or oils. Pustules on the face can also be caused by tinea infections. Lesions on the back are more problematic.


When they occur alone, staphylococcal folliculitis, miliaria (“heat rash”) or, uncommonly, malassezia folliculitis should be suspected. Bacterial culture, trial of an antistaphylococcal antibiotic, and observing the response to therapy will help in the differential diagnosis. In patients with HIV infection, folliculitis is common and may be either staphylococcal folliculitis or eosinophilic folliculitis.


Cyst formation, pigmentary changes in pigmented patients, severe scarring, and psychological problems may result.



1. Education of the patient

When scarring seems out of proportion to the severity of the lesions, clinicians must suspect that the patient is manipulating the lesions. It is essential that the patient be educated in a supportive way about this complication. Although there are exceptions, it is wise to let the patient know that at least 4–6 weeks will be required to see improvement and that old lesions may take months to fade. Therefore, improvement will be judged according to the number of new lesions forming after 6–8 weeks of therapy. Additional time will be required to see improvement on the back and chest, as these areas are slowest to respond. If hair pomades are used, they should contain glycerin and not oil. Avoid topical exposure to oils, cocoa butter (theobroma oil), and greases.

2. Diet

Foods do not cause or exacerbate acne.


Treatment of acne is based on the type and severity of lesions. Comedones require treatment different from that of pustules and cystic lesions. In assessing severity, take the sequelae of the lesions into account. Therefore, an individual who gets only two new lesions per month that scar or leave postinflammatory hyperpigmentation must be treated much more aggressively than a comparable patient whose lesions clear without sequelae. Soaps play little role in acne treatment, and unless the patient's skin is exceptionally oily, a mild soap should be used to avoid irritation that will limit the usefulness of other topicals, all of which are themselves somewhat irritating.

1. Topical retinoids

Tretinoin is very effective for comedonal acne or for treatment of the comedonal component of more severe acne, but its usefulness is limited by irritation. Start with 0.025% cream (not gel) and have the patient use it at first twice weekly at night, then build up to as often as nightly. A few patients cannot use even this low-strength preparation more than three times weekly but even that may cause improvement. A peasized amount is sufficient to cover the entire face. To avoid irritation, have the patient wait 20 minutes after washing to apply. Adapalene gel 0.1% and reformulated tretinoin (Renova, Retin A Micro, Avita) are other options for patients irritated by standard tretinoin preparations. Some patients—especially teenagers—do best on 0.01% gel. Although the absorption of tretinoin is minimal, its use during pregnancy is contraindicated. Some patients report photosensitivity with tretinoin. Patients should be warned that they may flare in the first 4 weeks of treatment. Tazarotene gel (0.05% or 0.1%) (Tazorac) is a topical retinoid approved for treatment of psoriasis and acne.

2. Benzoyl peroxide

Benzoyl peroxide products are available in concentrations of 2.5%, 4%, 5%, 8%, and 10%, but it appears that 2.5% is as effective as 10% and less irritating. In general, water-based and not alcohol-based gels should be used to decrease irritation.

3. Antibiotics

Use of topical antibiotics (see below) has been demonstrated to decrease comedonal lesions.

4. Comedo extraction

Open and closed comedones may be removed with a comedo extractor but will recur if not prevented by treatment.


Antibiotics are the mainstay for treatment of inflammatory acne. They may be used topically or orally. The oral antibiotics of choice are tetracycline and doxycycline. Minocycline is often effective in acne unresponsive or resistant to treatment with these antibiotics but it is expensive. Rarely, other antibiotics such as trimethoprim-sulfamethoxazole (one double-strength tablet twice daily), clindamycin (150 mg twice daily), or a cephalosporin (cefadroxil or cephalexin) may be tried. Topical clindamycin phosphate and erythromycin are also used (see below). Topicals are probably the equivalent of about 500 mg/d of tetracycline given orally, which is half the usual starting dose. Topical antibiotics are used in three situations: for mild papular acne that can be controlled by topicals alone, for patients who refuse or cannot tolerate oral antibiotics, or to wean patients under good control from oral to topical preparations. It has been recommended that switching or rotating antibiotics be avoided to decrease resistance and that courses of benzoyl peroxide be used on occasion.

1. Mild acne

The first choice of topical antibiotics in terms of efficacy and relative lack of induction of resistant P acnes is the combination of erythromycin or clindamycin with benzoyl peroxide topical gel. Clindamycin (Cleocin T) lotion (least irritating), gel, or solution, or one of the many brands of topical erythromycin gel or solution, may be used twice daily and the benzoyl peroxide in the morning. (A combination of erythromycin or clindamycin with benzoyl peroxide is available as a prescription item.) The addition of tretinoin 0.025% cream or 0.01% gel at night may be effective, since it works via a different mechanism.

2. Moderate acne

Tetracycline, 500 mg twice daily, doxycycline, 100 mg twice daily, and minocycline, 50–


100 mg twice daily, are all effective though minocycline is more expensive. When initiating minocycline therapy, start at 100 mg in the evening for 4–7 days, then 100 mg twice daily, to decrease the incidence of vertigo. Plan a return visit in 6 weeks and at 3–4 months after that. If the patient's skin is quite clear, instructions should be given for tapering the dose by 250 mg for tetracycline and erythromycin, by 100 mg for doxycycline, or by 50 mg for minocycline every 6–8 weeks—while treating with topicals— to arrive at the lowest systemic dose needed to maintain clearing. In general, lowering the dose to zero without other therapy results in prompt recurrence of acne. Tetracycline, minocycline, and doxycycline are contraindicated in pregnancy, but oral erythromycin may be used.

It is important to discuss the issue of contraceptive failure when prescribing antibiotics for women taking oral contraceptives. Women may need to consider using barrier methods as well, and should report breakthrough bleeding. Oral contraceptives or spironolactone (50–200 mg daily) may be added as an antiandrogen in women with antibiotic-resistant acne or in women in whom relapse occurs after isotretinoin therapy.

3. Severe acne

a. Isotretinoin (Accutane)

A vitamin A analog, isotretinoin is used for the treatment of severe cystic acne that has not responded to conventional therapy. Informed consent must be obtained before its use. A dosage of 0.5–1 mg/kg/d for 20 weeks for a cumulative dose of at least 120 mg/kg is usually adequate for severe cystic acne. Patients should b offered isotretinoin therapy before they experience significant scarring if they are not promptly and adequately controlled by antibiotics. The drug is absolutely contraindicated during pregnancy because of its teratogenicity; two serum pregnancy tests should be obtained before starting the drug in a female and every month thereafter. Sufficient medication for only 1 month should be dispensed. Two forms of effective contraception must be used. Side effects occur in most patients, usually related to dry skin and mucous membranes (dry lips, nosebleed, and dry eyes). If headache occurs, pseudotumor cerebri must be considered. Depression has been reported. Hypertriglyceridemia will develop in about 25% of patients, hypercholesterolemia in 15%, and a lowering of high-density lipoproteins in 5%. Minor elevations in liver function tests may develop in some patients. Fasting blood sugar may be elevated. Miscellaneous adverse reactions include decreased night vision, musculoskeletal or bowel symptoms, dry skin, thinning of hair, exuberant granulation tissue in lesions, and bony hyperostoses (seen only with very high doses or with long duration of therapy). Moderate to severe myalgias necessitate decreasing the dosage or stopping the drug. Laboratory tests to be performed in all patients before treatment and after 4 weeks on therapy include cholesterol, triglycerides, and liver function studies.

Elevations of liver enzymes and triglycerides return to normal upon conclusion of therapy. The drug may induce long-term remissions in 40–60%, or acne may recur that is more easily controlled with conventional therapy. Occasionally, acne does not respond or promptly recurs after therapy, but it may clear after a second course.

b. Intralesional injection

In otherwise moderate acne, intralesional injection of dilute suspensions of triamcinolone acetonide (2.5 mg/mL, 0.05 mL per lesion) will often hasten the resolution of deeper papules and occasional cysts.

c. Laser, dermabrasion

Cosmetic improvement may be achieved by excision and punch-grafting of deep scars and by abrasion of inactive acne lesions, particularly flat, superficial scars. The technique is not without untoward effects, since hyperpigmentation, hypopigmentation, grooving, and scarring have been known to occur. Dark-skinned individuals do poorly. Corrective surgery within 12 months after isotretinoin therapy may not be advisable. Active acne of all types can be treated with certain laser and photodynamic therapies. This can be considered when standard treatments are contraindicated or fail.


Acne vulgaris eventually remits spontaneously, but when this will occur cannot be predicted. The condition may persist throughout adulthood and may lead to severe scarring if left untreated. Patients treated with antibiotics continue to improve for the first 3–6 months of therapy. Relapse during treatment may suggest the emergence of resistant P acnes. The disease is chronic and tends to flare intermittently in spite of treatment. Remissions following systemic treatment with isotretinoin may be lasting in up to 60% of cases. Relapses after isotretinoin usually occur within 3 years and require a second course in up to 20% of patients.

Johnson BA et al: Use of systemic agents in the treatment of acne vulgaris. Am Fam Physician 2000;62:1823.

Ozolins M et al: Comparison of five antimicrobial regimens for treatment of mild to moderate inflammatory facial acne vulgaris in the community randomised controlled trial. Lancet 2004;364:2188.

Shalita AR et al: Effects of tazarotene 0.1% cream in the treatment of facial acne vulgaris: pooled results from two multicenter, double-blind, randomized, vehicle-controlled, parallel-group trials. Clin Ther 2004;26:1865.

Thiboutot D: Acne: hormonal concepts and therapy. Clin Dermatol 2004;22:419.

van Vloten WA et al: Selecting an oral contraceptive agent for the treatment of acne in women. Am J Clin Dermatol 2004;5:435.



  • A chronic facial disorder of middle-aged and older people.

  • P.118

  • A vascular component (erythema and telangiectasis) and a tendency to flush easily.

  • An acneiform component (papules and pustules) may also be present.

  • A glandular component accompanied by hyperplasia of the soft tissue of the nose (rhinophyma).

General Considerations

The pathogenesis of this disorder is not known. Topical corticosteroids can change trivial dermatoses of the face into perioral dermatitis and steroid rosacea. These occur predominantly in young women and may be confused with acne rosacea.

Clinical Findings

The cheeks, nose, and chin—at times the entire face— may have a rosy hue. No comedones are seen. Inflammatory papules are prominent, and there may be pustules. Associated seborrhea may be found. The patient often complains of burning or stinging with episodes of flushing. It is not uncommon for patients to have associated ophthalmic disease, including blepharitis and keratitis. This often requires systemic antibiotic therapy.

Differential Diagnosis

Rosacea is distinguished from acne by age, the presence of the vascular component, and the absence of comedones. The rosy hue of rosacea and telangiectases will pinpoint the diagnosis.


Medical management is effective only for the inflammatory papules and pustules and the erythema that surrounds them. The only satisfactory treatment for the telangiectasias is surgery. Rhinophyma (soft tissue and sebaceous hyperplasia of the nose) responds to surgical debulking. Rosacea is usually a lifelong condition, so maintenance therapy is required.


Metronidazole, 0.75% gel applied twice daily or 1% cream once daily, is the topical treatment of choice. If metronidazole is not tolerated, topical clindamycin (solution, gel, or lotion) used twice daily is effective. Five to 8 weeks of treatment are needed for significant response.


Tetracycline, 250 or 500 mg orally twice daily on an empty stomach, should be used when topical therapy is inadequate. Minocycline or doxycycline, 50–100 mg daily to twice daily, is also effective. Metronidazole or amoxicillin, 250–500 mg twice daily, may be used in refractory cases. Side effects are few, although metronidazole may produce a disulfiram-like effect when the patient ingests alcohol. Isotretinoin may succeed where other measures fail. A dosage of 0.5–1 mg/kg/d orally for 12–28 weeks is recommended. See precautions above.


Rosacea tends to be a stubborn and persistent process. With the regimens described above, it can usually be controlled adequately.

Powell FC: Rosacea. N Engl J Med 2005;352:793.

FOLLICULITIS (Including Sycosis)


  • Itching and burning in hairy areas.

  • Pustules in the hair follicles.

General Considerations

Folliculitis has multiple causes. It is frequently caused by staphylococcal infection and may be more common in the diabetic patient. When the lesion is deep-seated, chronic, and recalcitrant on the head and neck, it is called sycosis. Sycosis is usually propagated by the autoinoculation and trauma of shaving. The upper lip is particularly susceptible to involvement in men.

Gram-negative folliculitis, which may develop during antibiotic treatment of acne, may present as a flare of acne pustules or nodules. Klebsiella, Enterobacter, Escherichia coli, and Proteus have been isolated from these lesions.

“Hot tub folliculitis,” caused by Pseudomonas aeruginosa, is characterized by pruritic or tender follicular, pustular lesions occurring within 1–4 days after bathing in a hot tub, whirlpool, or public swimming pool. Rarely, systemic infections may result.

Nonbacterial folliculitis may also be caused by oils that are irritating to the follicle, and these may be encountered in the workplace (machinists) or at home (various cosmetics and cocoa butter or coconut oils).

Folliculitis may also be caused by occlusion, perspiration, and rubbing, such as that resulting from tight jeans and other heavy fabrics on the upper legs.

Folliculitis on the back that looks like acne but does not respond to acne therapy may be caused by the yeast M furfur. This infection may require biopsy for diagnosis.

Steroid acne may be seen during topical or systemic corticosteroid therapy.


A form of sterile folliculitis called eosinophilic folliculitis consisting of urticarial papules with prominent eosinophilic infiltration is common in patients with AIDS. It may appear first with institution of highly active antiretroviral therapy (HAART) and be mistaken for a drug eruption.

Pseudofolliculitis is caused by ingrowing hairs in the beard area. In this entity, the papules and pustules are located at the side of and not in follicles. It may be treated by growing a beard, by using chemical depilatories, or by shaving with a foil-guard razor. Laser hair removal is dramatically beneficial in patients with pseudofolliculitis, requires limited maintenance, and can be done on patients of any skin color. Pseudofolliculitis is a true medical indication for such a procedure and should not be considered cosmetic.

Clinical Findings

The symptoms range from slight burning and tenderness to intense itching. The lesions consist of pustules of hair follicles.

Differential Diagnosis

It is important to differentiate bacterial from nonbacterial folliculitis. The history is important for pinpointing the causes of nonbacterial folliculitis, and a Gram stain and culture are indispensable. One must differentiate folliculitis from acne vulgaris or pustular miliaria (heat rash) and from infections of the skin such as impetigo or fungal infections. Pseudomonas folliculitis is often suggested by the history of hot tub use. Eosinophilic folliculitis in AIDS often requires biopsy for diagnosis.


Abscess formation is the major complication of bacterial folliculitis.


Correct any predisposing local causes (eg, irritations of a mechanical or chemical nature). Control of blood glucose in diabetes may reduce the number of these infections. Be sure that the water in hot tubs and spas is treated properly with chlorine. If staphylococcal folliculitis is persistent, treatment of nasal or perineal carriage with rifampin, 600 mg daily for 5 days, or with topical mupirocin ointment 2% twice daily for 5 days, may help. Chronic oral clindamycin, 150–300 mg/d, is also effective in preventing recurrent staphylococcal folliculitis and furunculosis.



Anhydrous ethyl alcohol containing 6.25% aluminum chloride (Xerac AC), applied to lesions and environs, may be helpful, especially for chronic folliculitis of the buttocks.


Systemic antibiotics may be tried if the skin infection is resistant to local treatment, if it is extensive or severe and accompanied by a febrile reaction, if it is complicated, or if it involves the nose or upper lip. Extended periods of treatment (4–8 weeks or more) with antistaphylococcal antibiotics are required in some cases.

Hot tub pseudomonas folliculitis virtually always resolves without treatment but may be treated in adults with ciprofloxacin, 500 mg twice daily for 5 days.

Gram-negative folliculitis in acne patients may be treated with isotretinoin in compliance with all precautions discussed above (see Acne Vulgaris).

Folliculitis due to M furfur is treated with topical 2.5% selenium sulfide, 15 minutes daily for 3 weeks, or with oral ketoconazole, 200 mg daily for 7–14 days.

Eosinophilic folliculitis may be treated initially by the combination of potent topical corticosteroids and oral antihistamines. In more severe cases, treatment is with one of the following: topical permethrin (application for 12 hours every other night for 6 weeks); itraconazole, 200–400 mg daily; UVB or PUVA phototherapy; or isotretinoin, 0.5 mg/kg/d for up to 5 months. A remission may be induced by some of these therapies, but chronic treatment may be required.


Bacterial folliculitis is occasionally stubborn and persistent, requiring prolonged or intermittent courses of antibiotics. Corticosteroid folliculitis is treatable by acne therapy and resolves as corticosteroids are discontinued.

Cook-Bolden FE et al: Twice-daily applications of benzoyl peroxide 5%/clindamycin 1% gel versus vehicle in the treatment of pseudofolliculitis barbae. Cutis 2004;73:18.

Stulberg DL et al: Common bacterial skin infections. Am Fam Physician 2002;66:119.

MILIARIA (Heat Rash)


  • Burning, itching, superficial aggregated small vesicles, papules, or pustules on covered areas of the skin, usually the trunk.

  • More common in hot, moist climates.

  • Rare forms associated with fever and even heat prostration.


General Considerations

Miliaria is an acute dermatitis that occurs most commonly on the trunk and intertriginous areas. A hot, moist environment is the most frequent cause. Bedridden febrile patients are susceptible. Plugging of the ostia of sweat ducts occurs, with consequent ballooning and ultimate rupture of the sweat duct, producing an irritating, stinging reaction. Increase in numbers of resident aerobes, notably cocci, apparently plays a role. Drugs that enhance sweat gland function (eg, clonidine, β-blockers, opiates), may contribute.

Clinical Findings

The usual symptoms are burning and itching. In severe cases, fever, heat prostration, and even death may result. The lesions consist of small, superficial, red, thin-walled, discrete but closely aggregated vesicles (miliaria crystallina), papules (miliaria rubra), or vesicopustules or pustules (miliaria pustulosa). The reaction occurs most commonly on covered areas of the skin and virtually always affects the back in a hospitalized patient.

Differential Diagnosis

Miliaria is to be distinguished from drug rash and folliculitis.


Use of an antibacterial preparation such as chlorhexidine prior to exposure to heat and humidity may help prevent the condition. Susceptible persons should avoid exposure to hot, humid environments.


The patient should keep cool and wear light clothing. Triamcinolone acetonide, 0.1% in Sarna lotion, or a mid-potency corticosteroid in a lotion or cream—but not ointment—base, should be applied two to four times daily. Secondary infections (superficial pyoderma) are treated with dicloxacillin, 250 mg four times daily by mouth. Anticholinergic drugs given by mouth may be helpful in severe cases, eg, glycopyrrolate, 1 mg twice daily.


Miliaria is usually a mild disorder, but severe forms (tropical anhidrosis and asthenia) result from interference with the heat-regulating mechanism.

Haas N et al: Miliaria crystallina in an intensive care setting. Clin Exp Dermatol 2004;29:32.



  • Severe pruritus of vulva, anus, or body folds.

  • Superficial denuded, beefy-red areas with or without satellite vesicopustules.

  • Whitish curd-like concretions on the oral and vaginal mucous membranes.

  • Yeast on microscopic examination of scales or curd.

General Considerations

Mucocutaneous candidiasis is a superficial fungal infection that may involve almost any cutaneous or mucous surface of the body. It is particularly likely to occur in diabetics, during pregnancy, and in obese persons who perspire freely. Antibiotics and oral contraceptive agents may be contributory. Oral candidiasis may be the first sign of HIV infection (see Chapter 31).

Clinical Findings


Itching may be intense. Burning is reported, particularly around the vulva and anus. The lesions consist of superficially denuded, beefy-red areas in the depths of the body folds such as in the groin and the intergluteal cleft, beneath the breasts, at the angles of the mouth, and in the umbilicus. The peripheries of these denuded lesions are superficially undermined, and there may be satellite vesicopustules. Whitish, curd-like concretions may be present on mucosal lesions. Paronychia erosions may occur.


Clusters of budding cells and pseudohyphae can be seen under high power when skin scales or curd-like lesions have been cleared in 10% KOH. The organism may be isolated on Sabouraud's medium.

Differential Diagnosis

Intertrigo, seborrheic dermatitis, tinea cruris, “inverse psoriasis,” and erythrasma involving the same areas may mimic mucocutaneous candidiasis.


Systemic invasive candidiasis with candidemia may be seen with immunosuppression and in patients receiving broad-spectrum antibiotic and hypertonic glucose solutions, as in hyperalimentation. There may or may not be clinically evident mucocutaneous candidiasis.



Affected parts should be kept dry and exposed to air as much as possible. If possible, discontinue systemic antibiotics. For treatment of systemic invasive candidiasis, see Chapter 36.



1. Nails and skin

Apply clotrimazole solution 1% three or four times daily. Thymol 4% in ethanol applied once daily is an alternative. Nipple pain during breastfeeding may be due to candidiasis.

2. Vulvar and anal mucous membranes

For vaginal candidiasis, single-dose fluconazole (150 mg) is effective. Intravaginal clotrimazole, miconazole, terconazole, or nystatin may also be used. Long-term suppressive therapy may be required for recurrent or “intractable” cases. Non-albicans candidal species may be identified by culture in some refractory cases and may respond to oral itraconazole, 200 mg twice daily for 2–4 weeks.

3. Balanitis

This is most frequent in uncircumcised men, and candida usually plays a role. Topical nystatin ointment is the initial treatment if the lesions are mildly erythematous or superficially erosive. Soaking with dilute aluminum acetate for 15 minutes twice daily may quickly relieve burning or itching. Chronicity and relapses, especially after sexual contact, suggest reinfection from a sexual partner who should be treated. Severe purulent balanitis is usually due to bacteria. If it is so severe that phimosis occurs, oral antibiotics—some with activity against anaerobes—are required; if rapid improvement does not occur, urologic consultation is indicated.


Cases of cutaneous candidiasis range from the easily cured to the intractable and prolonged.

Amir L: Test your knowledge. Nipple pain in breastfeeding. Aust Fam Physician 2004;33:44.

Bielan B: What's your assessment? Candida balanitis. Dermatol Nurs 2003;15:134, 170.

Bielan B: What's your assessment? Candidiasis. Dermatol Nurs 2004;16:62.





  • Eruptions of evanescent wheals or hives.

  • Itching is usually intense but may on rare occasions be absent.

  • Special forms of urticaria have special features (dermographism, cholinergic urticaria, solar urticaria, or cold urticaria).

  • Most incidents are acute and self-limited over a period of 1–2 weeks.

  • Chronic urticaria (episodes lasting > 6 weeks) may have an autoimmune basis.

General Considerations

Urticaria can result from many different stimuli on an immunologic or nonimmunologic basis. The most common immunologic mechanism is hypersensitivity mediated by IgE, seen for most patients with acute urticaria; another involves activation of the complement cascade. Some patients with chronic urticaria demonstrate autoantibodies directed against mast cell IgE receptors, with histamine-releasing activity. Angiotensin-converting enzyme inhibitor and angiotensin II receptor antagonist therapy may be complicated by urticaria or angioedema. In general, extensive costly workups are not indicated in patients who have urticaria. A careful history and physical examination are more helpful.

Clinical Findings


Lesions are itchy red swellings of a few millimeters to many centimeters. The morphology of the lesions may vary over a period of minutes to hours, resulting in geographic or bizarre patterns. Individual lesions in true urticaria last less than 24 hours, and often only 2–4 hours. Angioedema is involvement of deeper subcutaneous tissue with swelling of the lips, eyelids, palms, soles, and genitalia. Angioedema is no more likely than urticaria to be associated with systemic complications such as laryngeal edema or hypotension. In cholinergic urticaria, triggered by a rise in core body temperature (hot showers, exercise), wheals are 2–3 mm in diameter with a large surrounding red flare. Cold urticaria is acquired or inherited and triggered by exposure to cold and wind (see Chapter 38).


Laboratory studies are not likely to be helpful in the evaluation of acute or chronic urticaria. The most common causes of acute urticaria are foods, infections, and medications. The cause of chronic urticaria is often not found. In patients with individual slightly purpuric lesions that persist past 24 hours, skin biopsy may confirm urticarial vasculitis. An autologous serum test may detect patients with an autoimmune basis for their chronic urticaria.

Differential Diagnosis

Papular urticaria resulting from insect bites persists for days. A central punctum can usually be seen. Streaked urticarial lesions may be seen in acute allergic plant dermatitis, eg, poison ivy, oak, or sumac. Contact urticaria may be caused by a host of substances, including chemicals, foods, and medications, and may be one


type of reaction to latex. Urticarial response to heat, sun, water, and pressure are quite rare. Urticarial vasculitis may be seen as part of serum sickness, associated with fever and arthralgia.

In hereditary angioedema, there is generally a positive family history and gastrointestinal or respiratory symptoms. Urticaria is not part of the syndrome, and lesions are not pruritic.



A detailed search by history for a cause of acute urticaria should be undertaken, and treatment may then be tailored to include the provocative condition. The chief causes are drugs—eg, aspirin, NSAIDs, morphine, and codeine; arthropod bites—eg, insect bites and bee stings (though the latter may cause anaphylaxis as well as angioedema); physical factors such as heat, cold, sunlight, and pressure; and, presumably, neurogenic factors, as in cholinergic urticaria induced by exercise, excitement, hot showers, etc.

Other causes may include penicillins and other medications; inhalants such as feathers and animal danders; ingestion of shellfish, tomatoes, or strawberries; injections of sera and vaccines; external contactants, including various chemicals and cosmetics; and infections such as viral hepatitis.


The mainstay of treatment initially includes H1 antihistamines (see above). Hydroxyzine, 10 mg twice daily to 25 mg three times daily, may be very useful if tolerated. Giving hydroxyzine as one dose of 50–75 mg at night may reduce sedation and other side effects. Cyproheptadine, 4 mg four times daily, may be especially useful for cold urticaria. “Nonsedating” or less sedating antihistamines are added if the generic sedating antihistamines are not effective. Fexofenadine is given in a dosage of 60 mg twice a day, or loratadine is given in a dosage of 10 mg/d. Cetirizine, a metabolite of hydroxyzine, is less sedating (13% of patients) and is given in a dosage of 10 mg/d.

Doxepin (a tricyclic antidepressant), 25–75 mg at bedtime, can be very effective in chronic urticaria. It has anticholinergic side effects.

H2 antihistamines in combination with H1 blockers may be helpful in patients with symptomatic dermatographism and to a lesser degree in chronic urticaria.

A few patients with chronic urticaria may respond to elimination of salicylates and tartrazine (coloring agent). Asymptomatic foci of infection—sinusitis, vaginal candidiasis, cholecystitis, and intestinal parasites—may rarely cause chronic urticaria. Systemic corticosteroids in a dose of about 40 mg daily will usually suppress acute and chronic urticaria. However, the use of corticosteroids is rarely indicated, since properly selected combinations of antihistamines with less toxicity are usually effective. Once corticosteroids are withdrawn, the urticaria virtually always returns if it had been chronic. Rather than using systemic corticosteroids in difficult cases, consultation should be sought from a dermatologist or allergist with experience in managing severe urticaria. Cyclosporine (3–5 mg/kg/d) may be effective in severe cases of autoimmune chronic urticaria.


Local treatment is rarely rewarding.


Acute urticaria usually lasts only a few days to 6 weeks. Half of patients whose urticaria persists for more than 6 weeks will have it for years.

Caproni M et al: Chronic idiopathic and chronic autoimmune urticaria: clinical and immunopathological features of 68 subjects. Acta Derm Venereol 2004;84:288.

Gaig P et al: Epidemiology of urticaria in Spain. J Investig Allergol Clin Immunol 2004;14:214.

Grattan CE et al: Chronic urticaria. J Am Acad Dermatol 2002;46:657.



  • Sudden onset of symmetric erythematous skin lesions with history of recurrence.

  • May be macular, papular, urticarial, bullous, or purpuric.

  • “Target” lesions with clear centers and concentric erythematous rings or “iris” lesions may be noted in erythema multiforme minor. These are rare in drug-associated erythema multiforme major (Stevens-Johnson syndrome).

  • Erythema multiforme minor on extensor surfaces, palms, soles, or mucous membranes. Erythema multiforme major favors the trunk.

  • Herpes simplex, systemic infection or disease, and drug reactions are often associated.

General Considerations

Erythema multiforme is an acute inflammatory skin disease. Erythema multiforme is divided clinically into minor and major types based on the clinical findings. Approximately 90% of cases of erythema multiforme minor follow outbreaks of herpes simplex. Erythema multiforme major (Stevens-Johnson syndrome) is marked by toxicity and involvement of two or more mucosal surfaces (often oral and conjunctival) and is most often caused by drugs, especially sulfonamides, NSAIDs, and anticonvulsants such as phenytoin. Mycoplasma pneumoniae


may trigger erythema multiforme major. Immunization for smallpox and acute HIV infection may also cause erythema multiforme. Erythema multiforme may also present as recurring oral ulceration, with skin lesions present in only half of the cases, and is diagnosed by oral biopsy. Since erythema multiforme may have its own prodrome, many medications taken for such symptoms have been implicated in its pathogenesis without definitive proof. As in all drug eruptions, the exposure to drugs associated with erythema multiforme may be systemic or topical; any agent should be considered a potential offender.

Clinical Findings


A classic target lesion, found most commonly in herpes-associated erythema multiforme, consists of three concentric zones of color change, most often found acrally on the hands and feet. Not all lesions will have this appearance. Drug-associated erythema multiforme is manifested by raised target-like lesions, with only two zones of color change and a central blister, or nondescript reddish or purpuric macules. In erythema multiforme major, mucous membrane ulcerations are present at two or more sites, causing pain on eating, swallowing, and urination.


Blood tests are not useful for diagnosis. Skin biopsy is diagnostic. Direct immunofluorescence studies are negative.

Differential Diagnosis

Urticaria and drug eruptions are the chief entities that must be differentiated from erythema multiforme minor. Individual lesions of true urticaria itch should come and go within 24 hours, are usually responsive to antihistamines, and do not affect the mucosa. In erythema multiforme major, the main differential diagnosis is paraneoplastic pemphigus. The presence of blisters is always worrisome and dictates the need for consultation. The differential diagnosis of blisters includes pemphigus, pemphigoid, and bullous drug eruptions. Skin biopsy is the mainstay of diagnosis.


The tracheobronchial mucosa and conjunctiva may be involved in severe cases with resultant scarring (StevensJohnson syndrome). Ophthalmologic consultation is recommended if ocular involvement is present.



Erythema multiforme major (Stevens-Johnson syndrome) with extensive denudation of skin is best treated in a burn unit. Otherwise, patients need not be admitted unless mucosal involvement interferes with hydration and nutrition. Patients who begin to blister should be seen daily. Immediate discontinuation of the inciting medication (before blistering occurs) improves prognosis and reduces the risk of death in erythema multiforme major.


Although there are no good data to support the use of corticosteroids in erythema multiforme major, they are still often prescribed. If corticosteroids are to be tried in more severe cases, they should be used early, before blistering occurs, and in moderate to high doses (prednisone, 100–250 mg) and stopped within days if there is no dramatic response. Intravenous immunoglobulin (IGIV) (0.75 g/kg/d for 4 days) may be used in severe cases. Oral and topical corticosteroids are useful in the oral variant of erythema multiforme. Oral acyclovir prophylaxis of herpes simplex infections may be effective in preventing recurrent herpes-associated erythema multiforme minor. Antistaphylococcal antibiotics are used for secondary infection, which is uncommon.


Topical therapy is not very effective in this disease. For oral lesions, 1% diphenhydramine elixir mixed with Kaopectate or with 1% dyclonine may be used as a mouth rinse several times daily.


Erythema multiforme minor usually lasts 2–6 weeks and may recur. Erythema multiforme major may be serious or even fatal in the most severe cases.

Bachot N et al: Intravenous immunoglobulin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis: a prospective noncomparative study showing no benefit on mortality or progression. Arch Dermatol 2003;139:33.

Chopra A et al: Stevens-Johnson syndrome after immunization with smallpox, anthrax, and tetanus vaccines. Mayo Clin Proc 2004;79:1193.

Colebunders R et al: Efavirenz-associated Stevens-Johnson syndrome. Infection 2004;32:306.

Prins C et al: Treatment of toxic epidermal necrolysis with highdose intravenous immunoglobulins: multicenter retrospective analysis of 48 consecutive cases. Arch Dermatol 2003; 139:26.

Schechner AJ et al: Acute human immunodeficiency virus infection presenting with erythema multiforme. Am J Emerg Med 2004;22:330.

3. ERYTHEMA MIGRANS (See also Chapter 34)

Erythema migrans is a unique cutaneous eruption that characterizes the localized or generalized early stage of Lyme disease. Three to 32 days (median: 7 days) after a


tick bite, there is gradual expansion of redness around the papule representing the bite site. The advancing border is usually slightly raised, warm, red to bluish-red, and free of any scale. Centrally, the site of the bite may clear, leaving only a rim of peripheral erythema, or it may become indurated, vesicular, or necrotic. The annular erythema usually grows to a median diameter of 15 cm (range: 3–68 cm, but virtually always > 5 cm). It is accompanied by a burning sensation in half of patients; rarely, it is pruritic or painful. Multiple secondary annular lesions similar in appearance to the primary lesion but without indurated centers and generally of smaller size will develop in 20% of patients. In the southeastern United States, similar lesions are seen in patients without evidence of Lyme borreliosis. The etiology of these cases is unclear, but they are not due to Borrelia.

Without treatment, erythema migrans and the secondary lesions fade in a median of 28 days, though some may persist for months. Ten percent of untreated patients experience recurrences over the ensuing months. Treatment with systemic antibiotics (see Table 34-4) is necessary to prevent systemic involvement. However, only 60–70% of those with systemic involvement experience erythema migrans.

Stanek G et al: Lyme borreliosis. Lancet 2003;362:1639.

Weed B: Lyme disease presenting with multiple erythema migrans lesions, an illustrative case. Int J Dermatol 2003;42: 715.

Wormser GP et al: Microbiologic evaluation of patients from Missouri with erythema migrans. Clin Infect Dis 2005;40: 23.




  • Edematous, spreading, circumscribed, hot, erythematous area, with or without vesicles or bullae.

  • Central face frequently involved.

  • Pain, chills, fever, and systemic toxicity may be striking.

General Considerations

Erysipelas is a superficial form of cellulitis that occurs classically on the cheek, caused by β-hemolytic streptococci.

Clinical Findings


The symptoms are pain, malaise, chills, and moderate fever. A bright red spot appears first, very often near a fissure at the angle of the nose. This spreads to form a tense, sharply demarcated, glistening, smooth, hot area. The margin characteristically makes noticeable advances in days or even hours. The lesion is somewhat edematous and can be pitted slightly with the finger. Vesicles or bullae occasionally develop on the surface. The lesion does not usually become pustular or gangrenous and heals without scar formation. The disease may complicate any break in the skin that provides a portal of entry for the organism.


Leukocytosis is almost invariably present; blood cultures may be positive.

Differential Diagnosis

Erysipeloid is a benign bacillary infection producing redness of the skin of the fingers or the backs of the hands in fishermen and meat handlers.


Unless erysipelas is promptly treated, death may result from extension of the process and systemic toxicity, particularly in the very young and in the aged.


Place the patient at bed rest with the head of the bed elevated. Intravenous antibiotics effective against group A β-hemolytic streptococci and staphylococci are indicated for the first 48 hours in all but the mildest cases. A 7-day course is completed with penicillin VK, 250 mg, dicloxacillin, 250 mg, or a first-generation cephalosporin, 250 mg, orally four times a day. Alternatives in penicillin-allergic patients are clindamycin or erythromycin, the latter only if the infection is known to be due to streptococci.


Erysipelas was at one time a life-threatening infection. It can now usually be quickly controlled with systemic penicillin or erythromycin therapy.

See references in the next section.



  • Edematous, expanding, erythematous, warm plaque with or without vesicles or bullae.

  • Lower leg is frequently involved.

  • Pain, chills, and fever are commonly present.

  • Septicemia may develop.


General Considerations

Cellulitis, a diffuse spreading infection of the dermis and subcutaneous tissue, is usually on the lower leg and most commonly due to gram-positive cocci, especially group A β-hemolytic streptococci and S aureus. Rarely, gram-negative rods or even fungi can produce a similar picture. In otherwise healthy persons, the most common portal of entry for lower leg cellulitis is tinea pedis of the toe web with fissuring. Injection drug use and open ulcerations may also be complicated by cellulitis. Cellulitis in the diabetic foot may be a major problem and is often associated with neuropathy and hyperkeratotic nodules from ill-fitting shoes and abnormal weight bearing.

Clinical Findings


Cellulitis begins as a small patch, which from its onset is tender. Swelling, erythema, and pain are often present. The lesion expands over hours, so that from onset to presentation is usually 6 to 36 hours. As the lesion grows, the patient becomes more ill with progressive chills, fever, and malaise. If septicemia develops, hypotension may develop followed by shock.


Leukocytosis or at least a neutrophilia (left shift) is present from early in the course. Blood cultures may be positive. If a central ulceration, pustule, or abscess is present, culture may be of value. Aspiration of the advancing edge has a low yield (20%) and is usually not performed. Instead, if an unusual organism is suspected and there is no loculated site to culture, a full thickness skin biopsy taken before antibiotics are given can be useful. Part is cultured and part processed for histologic evaluation with Gram stain. This technique is particularly useful in the immunocompromised patient.

Differential Diagnosis

Two potentially life threatening entities that can mimic cellulitis (ie, present with a painful, red, swollen lower extremity) include deep venous thrombosis and necrotizing fasciitis. The diagnosis of necrotizing fasciitis should be suspected in a patient who has a very toxic appearance, bullae, crepitus or anesthesia of the involved skin, overlying skin necrosis, and laboratory evidence of rhabdomyolysis (elevated creatine phosphokinase [CPK]) or disseminated intravascular coagulation. While these findings may be present with severe cellulitis and bacteremia, it is essential to rule out necrotizing fasciitis because rapid surgical debridement is essential. Other skin lesions that may resemble cellulitis include sclerosing panniculitis, an acute, exquisitely tender red plaque on the medial lower legs above the malleolus in patients with venous stasis or varicosities, and acute severe contact dermatitis on a limb, which produces erythema, vesiculation, and edema as seen in cellulitis, but with itching instead of pain. The erythema and edema are also more superficial than in cellulitis.


Intravenous or parenteral antibiotics may be required for the first 24–72 hours. In mild cases or following the initial parenteral therapy, dicloxacillin or cephalexin, 250–500 mg four times daily for 5–10 days, is usually adequate. In patients in whom intravenous treatment is not instituted, the first dose of oral antibiotic can be increased to 750–1000 mg to achieve rapid high blood levels.

Corwin P et al: Randomized controlled trial of intravenous antibiotic treatment for cellulitis at home compared with hospital. BMJ 2005;330:129.

Hepburn MJ et al: Comparison of short-course (5 days) and standard (10 days) treatment for uncomplicated cellulitis. Arch Intern Med 2004;164:1669.

Kettaneh A et al: Facial erysipelas after receiving acupuncture treatment. Scand J Infect Dis 2003;35:911.

Morris A: Cellulitis and erysipelas. Clin Evid 2004;(11):2133.

Roujeau JC et al: Chronic dermatomycoses of the foot as risk factors for acute bacterial cellulitis of the leg: a case-control study. Dermatology 2004;209:301.

Simonart T et al: The importance of serum creatine phosphokinase level in the early diagnosis and microbiological evaluation of necrotizing fasciitis. J Eur Acad Dermatol Venereol 2004;18:687.

Swartz MN: Cellulitis. N Engl J Med 2004;350:904.




  • Relapsing crops of bullae.

  • Often preceded by mucous membrane bullae, erosions, and ulcerations.

  • Superficial detachment of the skin after pressure or trauma variably present (Nikolsky's sign).

  • Acantholysis on biopsy.

  • Immunofluorescence studies are confirmatory.

General Considerations

Pemphigus is an uncommon intraepidermal blistering disease occurring on skin and mucous membranes. It is caused by autoantibodies to adhesion molecules expressed in the skin and mucous membranes (desmoglein 3, sometimes desmoglein 1 and plakoglobin in pemphigus vulgaris), and to a complex containing desmosomal proteins,


including desmoglein 1 (in pemphigus foliaceus). These autoantibodies cause acantholysis, the separation of epidermal cells from each other. The cause is unknown, and in the preantibiotic, presteroid era the condition, if untreated, was usually fatal within 5 years. The bullae appear spontaneously and are tender and painful when they rupture. If the lesions become extensive, the complications of the disease lead to great toxicity and debility. Drug-induced pemphigus from drugs including penicillamine, captopril, and others has been reported. There are several forms of pemphigus: pemphigus vulgaris and its variant, pemphigus vegetans; and the more superficially blistering pemphigus foliaceus and its variant, pemphigus erythematosus. All forms may occur at any age but most commonly in middle age. The vulgaris form begins in the mouth in over 50% of cases. The foliaceus form is especially apt to be associated with other autoimmune diseases, or it may be drug-induced. Paraneoplastic pemphigus, a unique form of the disorder, is associated with numerous types of benign and malignant neoplasms but most frequently non-Hodgkin's lymphoma.

Clinical Findings


Pemphigus is characterized by an insidious onset of flaccid bullae in crops or waves. In pemphigus vulgaris, lesions often appear first on the oral mucous membranes, and these rapidly become erosive. In some cases, erosions and crusts predominate over blisters. The scalp is another site of early involvement. Rubbing a cotton swab or finger laterally on the surface of uninvolved skin may cause easy separation of the epidermis (Nikolsky's sign).


The diagnosis is made by light microscopy and by direct and indirect immunofluorescence microscopy. Microscopically, acantholysis is the hallmark of pemphigus, but in some patients there may be eosinophilic spongiosis initially. Immunofluorescence microscopy shows intercellular deposits of IgG and C3 in the epidermis. Indirect immunofluorescence microscopy detects circulating pemphigus antibodies that correspond with disease activity and help in management.

Differential Diagnosis

Blistering diseases include erythema multiforme, drug eruptions, bullous impetigo, contact dermatitis, dermatitis herpetiformis, and bullous pemphigoid, but flaccid blisters are not typical of these diseases, and acantholysis is not seen. All of these diseases have clinical characteristics and different immunofluorescence test results that distinguish them from pemphigus.

Paraneoplastic pemphigus is clinically, histologically, and immunologically distinct from other forms of the disease. Oral erosions and erythematous plaques resembling erythema multiforme are seen. Survival rates are low because of the underlying malignancy.


Secondary infection commonly occurs; this is a major cause of morbidity and mortality. Disturbances of fluid, electrolyte, and nutritional intake can occur as a result of painful oral ulcers.



When the disease is severe, hospitalize the patient at bed rest and provide antibiotics and intravenous feedings as indicated. Anesthetic troches used before eating ease painful oral lesions.


Pemphigus very often requires systemic therapy as early in its course as possible. However, the main morbidity in this disease is due to the side effects of such therapy. Initial therapy is with systemic corticosteroids: prednisone, 60–80 mg daily. In all but the most mild cases, a steroid-sparing agent is added from the beginning, since the course of the disease is long and the steroid-sparing agents take several weeks to exert their activity. Azathioprine (100–200 mg daily) or mycophenolate mofetil (1–1.5 g twice daily) is used most frequently, the latter seeming to be the most reliable and recommended for most cases. In refractory cases, monthly IGIV at 2 g/kg intravenously over 3 days is useful and has replaced high-dose corticosteroids plus cyclophosphamide and pulse intravenous corticosteroids as rescue therapy. Increased risk of thromboembolism is associated with IGIV therapy in these doses. In pemphigus foliaceus and mild cases of pemphigus vulgaris, tetracycline, 500 mg, and nicotinamide, 500 mg, three times daily, may be tried. Dapsone may also be tried as a steroid-sparing agent, especially in pemphigus foliaceus.


In patients with limited disease, skin and mucous membrane lesions should be treated with topical corticosteroids. Complicating infection requires appropriate systemic and local antibiotic therapy.


The course tends to be chronic in most patients, though about one-third appear to experience remission. Infection is the most frequent cause of death, usually from S aureus septicemia.

Bystryn JC et al: Treatment of pemphigus with intravenous immunoglobulin. J Am Acad Dermatol 2002;47:358.

Sami N et al: Influence of IVIG therapy on autoantibody titers to desmoglein 1 in patients with pemphigus foliaceus. Clin Immunol 2002;105:192.

Sauret J et al: Rupturing bullae not responding to antibiotics. J Fam Pract 2004;53:981. Erratum in J Fam Pract 2005; 54:36.



Many other skin disorders are characterized by formation of bullae, or blisters. These include bullous pemphigoid, cicatricial pemphigoid, dermatitis herpetiformis, and pemphigoid gestationis.

Bullous Pemphigoid

Bullous pemphigoid is a relatively benign pruritic disease characterized by tense blisters in flexural areas, usually remitting in 5 or 6 years, with a course characterized by exacerbations and remissions. Most affected persons are over the age of 60 (often in their 70s or 80s), and men are affected twice as frequently as women. The appearance of blisters may be preceded by urticarial or edematous lesions for months. Oral lesions are present in about one-third of affected persons. The disease may occur in various forms, including localized, vesicular, vegetating, erythematous, erythrodermic, and nodular. There is no statistical association with internal malignant disease.

The diagnosis is made by biopsy and direct immunofluorescence examination. Light microscopy shows a subepidermal blister. With direct immunofluorescence, IgG and C3 are found at the dermal-epidermal junction. If the patient has only a few blisters, ultrapotent corticosteroids may be adequate. Prednisone at dosages of 40–80 mg/d is often used to achieve rapid control of more widespread disease. Although slower in onset of action, tetracycline or erythromycin, 500 mg three times daily, alone or combined with nicotinamide—not nicotinic acid or niacin!—(up to 1.5 g/d), if tolerated, may control the disease in patients who cannot use corticosteroids or may allow decreasing or eliminating corticosteroids after control is achieved. Dapsone is particularly effective in mucous membrane pemphigoid. If these drugs are not effective, methotrexate, 5–25 mg weekly, or azathioprine, 50 mg one to three times daily, may be used as steroid-sparing agents. Mycophenolate mofetil (1 g twice daily) or IGIV as used for pemphigus vulgaris may be used in refractory cases.

Ahmed AR: Intravenous immunoglobulin therapy for patients with bullous pemphigoid unresponsive to conventional immunosuppressive treatment. J Am Acad Dermatol 2001;45: 825.

Fernandez-Viadero C et al: Blisters in a nursing home: bullous pemphigoid more often than we think? J Am Geriatr Soc 2004;52:1405.

Wollina U: Treatment of bullous pemphigoid: what's new? J Eur Acad Dermatol Venereol 2003;17:623.

Herpes (Pemphigoid) Gestationis

Herpes gestationis occurs in about 1 in 50,000–60,000 pregnancies. The vesicles and bullae often appear first in periumbilical distribution, and there may be erythematous papules and plaques. It usually begins in the fifth or sixth month of pregnancy, or the onset may be delayed to the postpartum period. The disease is self-limited, but it may recur in subsequent pregnancies. Use of estrogens or progesterone or the onset of menses may trigger flare-ups. The risks to mother and fetus appear to be limited but include an increase in prematurity and small-for-gestational-age infants. Blisters are subepidermal, with eosinophils present. Direct immunofluorescence shows C3 at the basement membrane zone in most cases. IgG is found less often.

Corticosteroids are the treatment of choice and are sometimes effective when used topically only.

Wollina U et al: Itching stretch marks and bullous lesions in a pregnant woman. Int J Dermatol 2004;43:752.




  • Verrucous papules anywhere on the skin or mucous membranes, usually no larger than 1 cm in diameter.

  • Prolonged incubation period (average 2–18 months). Spontaneous “cures” are frequent (50% at 2 years for common warts).

  • “Recurrences” (new lesions) are frequent.

General Considerations

Warts are caused by human papillomaviruses (HPVs). The type of mucocutaneous surface infected and the morphology of the wart are closely related to the HPV type causing the infection. Especially in genital warts, simultaneous infection with numerous wart types is common. Genital HPVs are divided into low-risk and high-risk types depending on the likelihood of their association with cervical and anal cancer.

Clinical Findings

There are usually no symptoms. Tenderness on pressure occurs with plantar warts; itching occurs with anogenital warts. Occasionally a wart will produce mechanical obstruction (eg, nostril, ear canal, urethra).

Warts vary widely in shape, size, and appearance. Flat warts are most evident under oblique illumination. Subungual warts may be dry, fissured, and hyperkeratotic and may resemble hangnails or other nonspecific changes. Plantar warts resemble plantar corns or calluses.


Differential Diagnosis

Some warty-looking lesions are actually hypertrophic actinic keratoses or squamous cell carcinomas. Some genital warty lesions may be due to secondary syphilis (condylomata lata). The lesions of molluscum contagiosum may be mistaken for warts, especially when they are very large in immunocompromised persons. Seborrheic keratosis may also be confused with warts. In AIDS, wart-like lesions may be caused by varicella zoster virus.


The use of condoms may reduce transmission of genital warts. A person with flat warts should be educated about the infectivity of warts and advised not to scratch or traumatize the areas. Using an electric shaver may prevent autoinoculation.


Treatment is aimed at inducing “wart-free” intervals for as long as possible without scarring, since no treatment can guarantee a remission or prevent recurrences. In immunocompromised patients, the goal is even more modest, ie, to control the size and number of lesions present.


For common warts of the hands, patients are usually offered liquid nitrogen or keratolytic agents. The former may work in fewer treatments but requires office visits and is painful. Keratolytic agents are irritating but effective and usually painless if used correctly. They can be used at home but must be applied almost daily for 8–12 weeks for maximum effect.

1. Liquid nitrogen

Liquid nitrogen is applied to achieve a thaw time of 20–45 seconds. Two freezethaw cycles are given every 2–4 weeks for several visits. Scarring will occur if it is used incorrectly or too aggressively. For example, the face, dorsal hands, and legs are more sensitive than the palms. Improper use along the sides of the fingers has been reported to cause nerve damage and paresthesias. Liquid nitrogen may cause permanent depigmentation in darkly pigmented individuals. It is useful on penile warts and on filiform warts involving the face and body. Liquid nitrogen may be used for condylomas, but snipping of lesions followed by light electrodesiccation is more effective.

2. Keratolytic agents and occlusion

Salicylic acid products may be used against common warts or plantar warts. They are applied then occluded. Plantar warts may be treated by applying a 40% salicylic acid plaster (Mediplast) after paring. The plaster may be left on for 5–6 days, then removed, the lesion pared down, and another plaster applied. Although it may take weeks or months to eradicate the wart, the method is safe and effective with almost no side effects. Chronic occlusion alone with water-impermeable tape (duct tape, adhesive tape) for months may be effective.

3. Podophyllum resin

Anogenital warts are often initially treated by painting each wart carefully (protecting normal skin) every 2–3 weeks with 25% podophyllum resin (podophyllin) in compound tincture of benzoin. Pregnant patients should not be so treated. The purified active component of the resin, podofilox, is available for use at home twice daily 3 consecutive days a week for cycles of 4–6 weeks. It is less irritating and more effective than podophyllum resin. After a single 4-week cycle, 45% of patients were wart-free; but of these, 60% relapsed at 6 weeks. Thus, multiple cycles of treatment are often necessary.

4. Imiquimod

A 5% cream of this local interferon inducer has moderate activity in clearing external genital warts. Seventy-seven percent of women and 40% of men with external genital warts had complete clearing of their lesions, and 90% and 74%, respectively, had greater than 50% reduction in their warts. The superior response in women may relate to enhanced penetration of the moist skin of the vulva as compared with the penile shaft. Treatment is once daily on 3 alternate days per week. Response may be slow, with patients who eventually cleared having responses at 8 weeks (44%) or 12 weeks (69%). Once cleared, about 13% had recurrences in the short term.

There is less pregnancy risk than with podophyllum resin (category B versus category X with podophyllin). It is more expensive than podophyllotoxin, but given the high rate of response in women and its safety and low relapse rate, it appears to be the “patient-administered” treatment of choice in women. In men, the more rapid response, lower cost, and similar efficacy make podophyllotoxin the initial treatment of choice, with imiquimod used for recurrences or refractory cases. Imiquimod has no demonstrated efficacy for—and should not be used to treat—plantar or common warts.

5. Operative removal

Plantar warts may be removed by blunt dissection. Local anesthetic is injected into the base, and the wart is then removed with a curette or scissors or by shaving off at the base of the wart with a scalpel. Trichloroacetic acid or Monsel's solution on a tightly wound cotton-tipped applicator may be painted on the wound, or light electrocautery may be used. Excision of warts, however, may result in a permanent painful scar on the foot and is not recommended. For genital warts, snip biopsy (scissors) removal followed by light electrocautery is more effective than cryotherapy but may scar. It is often preferred by patients with pedunculated or large lesions that require multiple cryotherapy or podophyllin treatments for removal.

6. Laser therapy

The CO2 laser is effective for treating recurrent warts, periungual warts, plantar warts, and condylomata acuminata. It leaves open wounds that must fill in with granulation tissue over 4–6 weeks and is best reserved for warts resistant to all other modalities. Lasers with emissions of 585, 595, or 532 nm may also be used every 3–4 weeks to gradually


ablate common plantar warts. This is no more effective than cryotherapy in controlled trials. For genital warts, it has not been shown that laser therapy is more effective than electrosurgical removal.

7. Other agents

Bleomycin diluted to 1 unit/mL may be injected into warts. It has been shown to have a high cure rate for plantar and common warts. It should not be used on digital warts because of the potential complications of Raynaud's phenomenon, nail loss, and terminal digital necrosis.


Squaric acid dibutylester may be effective. It is applied in a concentration of 0.2–2% directly to the warts from once weekly to five times weekly to induce a mild contact dermatitis. Between 60% and 80% of warts clear over 10–20 weeks. Injection of candida antigen may be used in the same way.


Soaking warts in hot (42.2 C) water for 10–30 minutes daily for 6 weeks has resulted in dramatic involution in some cases.


There is a striking tendency to the development of new lesions. Warts may disappear spontaneously or may be unresponsive to treatment.

Focht DR 3rd et al: The efficacy of duct tape vs cryotherapy in the treatment of verruca vulgaris (the common wart). Arch Pediatr Adolesc Med 2002;156:971.

Gibbs S et al: Local treatments for cutaneous warts: systematic review. BMJ 2002;325:461.

Manhart LE et al: Do condoms prevent genital HPV infection, external genital warts or cervical neoplasia? A meta-analysis. Sex Transm Dis 2002;29:725.

Wiley DJ et al: External genital warts: diagnosis, treatment and prevention. Clin Infect Dis 2002;35(Suppl 2):S210.


Callosities and corns are caused by pressure and friction due to faulty weight-bearing, orthopedic deformities, improperly fitting shoes, or neuropathies.

Tenderness on pressure and “after-pain” are the only symptoms. The hyperkeratotic well-localized overgrowths always occur at pressure points. Fingerprint lines are preserved over the surface (not so in warts). When the surface is shaved with a 15 blade, a glassy core is found (which differentiates these disorders from plantar warts, which have multiple capillary bleeding points or black dots when pared). A soft corn often occurs laterally on the proximal portion of the fourth toe as a result of pressure against the bony structure of the interphalangeal joint of the fifth toe.

Treatment consists of correcting mechanical abnormalities that cause friction and pressure. Shoes must be properly fitted and orthopedic deformities corrected. Callosities may be removed by careful paring of the callus after a warm water soak or with keratolytic agents as found in various brands of corn pads.

Plantar hyperkeratosis of the heels can be treated successfully by using 20% urea (Ureacin 20) or 12% lactic acid (Lac-Hydrin) or combinations nightly and a pumice stone after soaking in water.

Women who tend to form calluses and corns should not wear confining footgear and high-heeled shoes. Callosities on diabetic feet, especially in the setting of hyposensate neuropathy, can be a major problem and the value of early management to prevent complications is very important.

Filippo JS et al: The nonresponding “wart.” Paring with a scalpel may reveal a different lesion. Postgrad Med 2003;114:57.

Pataky Z et al: The impact of callosities on the magnitude and duration of plantar pressure in patients with diabetes mellitus. A callus may cause 18,600 kilograms of excess plantar pressure per day. Diabetes Metab 2002;28:356.


Molluscum contagiosum, caused by a poxvirus, presents as single or multiple rounded, dome-shaped, waxy papules 2–5 mm in diameter that are umbilicated. Lesions at first are firm, solid, and flesh-colored but upon reaching maturity become softened, whitish, or pearly gray and may suppurate. The principal sites of involvement are the face, lower abdomen, and genitals.

The lesions are autoinoculable and spread by wet skin-to-skin contact. In sexually active individuals, they may be confined to the penis, pubis, and inner thighs and are considered a sexually transmitted disease.

Molluscum contagiosum is common in patients with AIDS, usually with a helper T cell count < 100/ mcL. Extensive lesions tend to develop over the face and neck as well as in the genital area.

The diagnosis is easily established in most instances because of the distinctive central umbilication of the dome-shaped lesion. The best treatment is by curettage or applications of liquid nitrogen as for warts—but more briefly, since molluscum contagiosum is more responsive to therapy than warts. When lesions are frozen, the central umbilication often becomes more apparent. Light electrosurgery with a fine needle is also effective. It has been estimated that individual lesions persist for about 2 months. They are difficult to eradicate in patients with AIDS unless immunity improves, in which case spontaneous clearing may occur.

Baxter KF et al: Topical cidofovir and cryotherapy—combination treatment for recalcitrant molluscum contagiosum in a patient with HIV infection. J Eur Acad Dermatol Venereol 2004;18:330.


Lerbaek A et al: Facial eruption of molluscum contagiosum during topical treatment of atopic dermatitis with tacrolimus. Br J Dermatol 2004;150:1210.

Scott PM: Curettage for molluscum contagiosum. JAAPA 2002;15:53.



  • Pearly papule, erythematous patch > 6 mm, or nonhealing ulcer, in sun exposed areas (face, trunk, lower legs).

  • History of bleeding.

  • Fair-skinned person with a history of sun exposure (often intense, intermittent).

General Considerations

Basal cell carcinomas are the most common form of cancer. They occur on sun-exposed skin in otherwise normal fair-skinned individuals; ultraviolet light is the cause. The most common presentation is a papule or nodule that may have a central scab or erosion. Occasionally the nodules have stippled pigment (pigmented basal cell carcinoma). Intradermal nevi without pigment on the face of older white individuals may resemble basal cell carcinomas. Basal cell carcinomas grow slowly, attaining a size of 1–2 cm or more in diameter, often after years of growth. There is a waxy, “pearly” appearance, with telangiectatic vessels easily visible. It is the pearly or translucent quality of these lesions that is most diagnostic, a feature best appreciated if the skin is stretched. Less common types include morpheaform or scar-like lesions. These are hypopigmented, somewhat thickened plaques. On the back and chest, basal cell carcinomas appear as reddish, somewhat shiny, scaly patches.

Clinicians should examine the skin routinely, looking for bumps, patches, and scabbed lesions. When examining the face, look at the eyelid margins and medial canthi, the nose and alar folds, the lips, and then around and behind the ears. While metastases almost never occur, therapy of basal cell carcinomas may cause significant cosmetic deformity in these areas, particularly for inadequately treated or recurrent lesions. Neglected lesions may ulcerate and produce great destruction. Basal cell carcinomas of the medial canthi are particularly dangerous. Recurrent lesions around the nose and ears may track along cartilage underneath the skin, requiring treatment of much more extensive areas than are apparent from inspection.


Lesions suspected to be basal cell carcinomas should be biopsied, by shave or punch biopsy. Therapy is then aimed at eradication with minimal cosmetic deformity, often by excision and suturing with recurrence rates of 5% or less. The technique of three cycles of curettage and electrodesiccation depends on the skill of the operator and is not recommended for head and neck lesions. After 4–6 weeks of healing, it leaves a broad, hypopigmented, at times hypertrophic scar. Radiotherapy is effective and sometimes appropriate for older individuals (over 65), but recurrent tumors after radiation therapy are more difficult to treat and may be more aggressive. Radiation therapy is the most expensive method to treat basal cell carcinoma and should only be used if other treatment options are not appropriate. Mohs surgery—removal of the tumor followed by immediate frozen section histopathologic examination of margins with subsequent reexcision of tumor-positive areas and final closure of the defect—gives the highest cure rates (98%) and results in least tissue loss. It is appropriate therapy for tumors of the eyelids or for recurrent lesions, or where tissue sparing is needed for cosmesis. Patients with basal cell carcinomas must be followed to detect new or recurrent lesions.

Diepgen TL et al: The epidemiology of skin cancer. Br J Dermol 2002;146(Suppl 61):1.

Marks R et al: Efficacy and safety of 5% imiquimod cream in treating patients with multiple superficial basal cell carcinomas. Arch Dermatol 2004;140:1284.



  • Nonhealing ulcer or warty nodule.

  • Skin damage due to long-term sun exposure.

  • Common in fair-skinned organ transplant recipients.

Squamous cell carcinoma usually occurs subsequent to prolonged sun exposure on exposed parts in fairskinned individuals who sunburn easily and tan poorly. It may arise from an actinic keratosis. The lesions appear as small red, conical, hard nodules that occasionally ulcerate. The frequency of metastasis is not precisely known, though metastatic spread is said to be less likely with squamous cell carcinoma arising out of actinic keratoses than with those that arise de novo. In actinically induced squamous cell cancers, rates of metastasis are estimated from retrospective studies to be 3–7%. Squamous cell carcinomas of the lip, oral cavity, tongue, and genitalia have much higher rates of metastasis and require special management.

Keratoacanthomas most often act in benign fashion but resemble squamous cell carcinoma histologically and for all practical purposes should be treated as though they were skin cancers.


Examination of the skin and therapy are essentially the same as for basal cell carcinoma. The preferred treatment of squamous cell carcinoma is excision. Electrodesiccation and curettage and x-ray radiation may be used for some lesions, and fresh tissue microscopically controlled excision (Mohs) is recommended for high-risk lesions (lips, temples, ears, nose) and for recurrent tumors. Some keratoacanthomas respond to intralesional injection of fluorouracil or methotrexate, but they must be excised if they do not. Follow-up for squamous cell carcinoma must be more frequent and thorough than for basal cell carcinoma, starting at every 3 months, with careful examination of lymph nodes. In addition, palpation of the lips is essential to detect hard or indurated areas that represent early squamous cell carcinoma. All such cases must be biopsied. Multiple squamous cell carcinomas are very common on the sun-exposed skin of organ transplant patients. The intensity of immunosuppression, not the use of any particular immunosuppressive agent, is the primary risk factor in determining the development of skin cancer after transplant. The tumors begin to appear after 5 years of immunosuppression. Regular dermatologic evaluation in at-risk organ transplant recipients is recommended. Biologic behavior of skin cancer in organ transplant recipients may be aggressive, and careful management is required.

Fortina AB et al: Immunosuppressive level and other risk factors for basal cell carcinoma and squamous cell carcinoma in heart transplant recipients. Arch Dermatol 2004;140:1079.

Garner KL et al: Basal and squamous cell carcinoma. Prim Care 2000;27:447.

JAMA patient page: Skin cancer. JAMA 1999;281:676.




  • Pruritic, violaceous, flat-topped papules with fine white streaks and symmetric distribution.

  • Lacy lesions of the buccal mucosa.

  • Commonly seen along linear scratch marks (Koebner phenomenon) on anterior wrists, penis, legs.

  • Histopathologic examination is diagnostic.

General Considerations

Lichen planus is an inflammatory pruritic disease of the skin and mucous membranes characterized by distinctive papules with a predilection for the flexor surfaces and trunk. The three cardinal findings are typical skin lesions, mucosal lesions, and histopathologic features of band-like infiltration of lymphocytes in the dermis. Drugs causing lichen planus-like reactions include gold, streptomycin, tetracycline, chloroquine, quinacrine, quinidine, NSAIDs, phenothiazines, and hydrochlorothiazide. Hepatitis C infection is found with greater frequency in lichen planus patients than in controls. Allergy to mercury amalgams can trigger oral lesions identical to lichen planus.

Clinical Findings

Itching is mild to severe. The lesions are violaceous, flat-topped, angulated papules, 1–4 mm in diameter, discrete or in clusters, with very fine white streaks (Wickham's striae) on the flexor surfaces of the wrists and on the penis, lips, tongue, and buccal and vaginal mucous membranes. The papules may become bullous or ulcerated. The disease may be generalized. Mucosal lichen planus has been reported in the genital and anorectal areas, the gastrointestinal tract, the bladder, the larynx, and the conjunctiva. Mucous membrane lesions have a lacy white network overlying them that may be confused with leukoplakia. The Koebner phenomenon (appearance of lesions in areas of trauma) may be seen.

A special form of lichen planus is the erosive or ulcerative variety. On palms and soles, it can be disabling. It is a major problem in the mouth or genitalia, and squamous cell carcinoma develops in 5% of patients with erosive oral or genital lichen planus.

Differential Diagnosis

Lichen planus must be distinguished from similar lesions produced by medications (see above) and other papular lesions such as psoriasis, lichen simplex chronicus, and syphilis. Lichen planus on the mucous membranes must be differentiated from leukoplakia. Erosive oral lesions require biopsy and often direct immunofluorescence for diagnosis since lichen planus may simulate other erosive diseases. Histologic examination may make the distinction from graft-versushost disease and in some cases from lichen planus-like drug eruptions.



Superpotent topical corticosteroids applied twice daily are most helpful for localized disease in nonflexural areas. Alternatively, high-potency corticosteroid cream or ointment may be used nightly under thin pliable plastic film.

Topical tacrolimus appears effective in oral and vaginal erosive lichen planus, but long-term therapy is required to prevent relapse. If the erosive lichen planus lesions are adjacent to a mercury containing amalgam,


removal of the amalgam may result in clearing of the erosions.


Corticosteroids (Chapter 26) may be required in severe cases or in circumstances where the most rapid response to treatment is desired. Unfortunately, relapse almost always occurs as the corticosteroids are tapered, making systemic corticosteroid therapy an impractical option for the management of chronic lichen planus.

Isotretinoin and acitretin by mouth appear to be effective in some cases of oral and cutaneous lichen planus.

PUVA may be effective treatment for lichen planus.


Lichen planus is a benign disease, but it may persist for months or years and may be recurrent. Hypertrophic lichen planus and oral lesions tend to be especially persistent, and neoplastic degeneration has been described in chronically eroded lesions.

Byrd JA et al: Response of oral lichen planus to topical tacrolimus in 37 patients. Arch Dermatol 2004;140:1508.

Jensen JT et al: Patient satisfaction after the treatment of vulvovaginal erosive lichen planus with topical clobetasol and tacrolimus: a survey study. Am J Obstet Gynecol 2004;190: 1759.

Laeijendecker R et al: Oral lichen planus and allergy to dental amalgam restorations. Arch Dermatol 2004;140:1434.

Popkin DL et al: Widespread annular eruption in a black man— quiz case. Arch Dermatol 2005;141:93.


General Considerations

Before 1980 in the United States, this rare malignant skin lesion was seen mostly in elderly white men, had a chronic clinical course, and was rarely fatal. Kaposi's sarcoma occurs endemically in an often aggressive form in young black men of equatorial Africa, but it is rare in American blacks. Kaposi's sarcoma continues to occur largely in homosexual men with HIV infection as an AIDS-defining illness. Kaposi's sarcoma may complicate immunosuppressive therapy, and stopping the immunosuppression may result in improvement. Human herpes virus 8 (HHV-8), or Kaposi's sarcoma-associated herpes virus (KSHV), is universally present in all forms of Kaposi's sarcoma. The virus is present in the skin lesions and circulating B lymphocytes of persons with Kaposi's sarcoma but uncommonly in their normal skin. A serologic test is available to detect infection with this virus, but its sensitivity is insufficient for commercial use at this time.

Red or purple plaques or nodules on cutaneous or mucosal surfaces are characteristic. Kaposi's sarcoma commonly involves the gastrointestinal tract, but in asymptomatic patients these lesions are not sought or treated. Pulmonary Kaposi's sarcoma may be life-threatening and is managed aggressively. The incidence of AIDS-associated Kaposi's sarcoma is diminishing.


For Kaposi's sarcoma in the elderly, palliative local therapy with intralesional chemotherapy or radiation is usually all that is required. In the setting of iatrogenic immunosuppression, the treatment of Kaposi's sarcoma is primarily reduction of doses of immunosuppressive medications. In AIDS-associated Kaposi's sarcoma, the patient should first be given effective anti-HIV antiretrovirals (including a protease inhibitor), because in most cases this treatment alone is associated with improvement. Other therapeutic options include cryotherapy or intralesional vinblastine (0.1–0.5 mg/mL) for cosmetically objectionable lesions; radiation therapy for accessible and space-occupying lesions; and laser surgery for certain intraoral and pharyngeal lesions. Systemic chemotherapy is indicated in patients with rapidly progressive skin disease (more than ten new lesions per month), with edema or pain, and with symptomatic visceral disease or pulmonary disease. Liposomal doxorubicin is highly effective in controlling these cases and has considerably less toxicity—and greater efficacy—than anthracycline monotherapy or combination chemotherapeutic regimens.

Antman K et al: Kaposi's sarcoma. N Engl J Med 2000;342:1027.

Cheung TW: AIDS-related cancer in the era of highly active antiretroviral therapy (HAART): a model of the interplay of the immune system, virus, and cancer. “On the offensive—the Trojan Horse is being destroyed”—Part A: Kaposi's sarcoma. Cancer Invest 2004;22:774.

Dal Maso L et al: Classic Kaposi's sarcoma in Italy, 1985–1998. Br J Cancer 2005;92:188.

Lim ST et al: Weekly docetaxel is safe and effective in the treatment of advanced-stage acquired immunodeficiency syndrome-related Kaposi sarcoma. Cancer 2005;103:417.

PRURITUS (Itching)

Pruritus is a disagreeable sensation that provokes a desire to scratch. It is modulated by central factors, including cortical ones. Not all cases of pruritus are mediated by histamine.

Although many cases of generalized pruritus can be attributed to dry skin—whether naturally occurring and precipitated or aggravated by climatic conditions or arising from disease states—there are many other causes: scabies, dermatitis herpetiformis, atopic dermatitis, pruritus vulvae et ani, miliaria, insect bites, pediculosis, contact dermatitis, drug reactions, urticaria, urticarial eruptions of pregnancy, psoriasis, lichen planus, lichen simplex chronicus, exfoliative dermatitis,


folliculitis, bullous pemphigoid, and fiberglass dermatitis.

Persistent pruritus not explained by cutaneous disease should prompt a staged workup for systemic causes. Perhaps the most common cause of pruritus associated with systemic disease is uremia in conjunction with hemodialysis. Both this condition and the pruritus of liver disease may be helped by phototherapy with ultraviolet B or PUVA. Naltrexone and nalmefene have been shown to relieve the pruritus of liver disease. Naltrexone is not effective in pruritus associated with renal failure, but gabapentin may be effective. Endocrine disorders such as hypothyroidism or hyperthyroidism, psychiatric disturbances, lymphoma, leukemia, and other internal malignant disorders, iron deficiency anemia, and certain neurologic disorders may also cause pruritus. Antihistamines reduce pruritus only by their sedating effect (except in urticaria). Nonsedating, second generation antihistamines are of no value in nonurticarial pruritus.


Elimination of external factors and irritating agents may give complete relief from pruritus. Pruritus accompanying specific skin disease will subside when the disease is controlled. Idiopathic pruritus and that accompanying serious internal disease may not respond to any type of therapy.

Bellmann R et al: Treatment of intractable pruritus in drug induced cholestasis with albumin dialysis: a report of two cases. ASAIO 2004;50:387.

Clarke P: Why am I so itchy? Aust Fam Physician 2004;33:489.

Crownover BK et al: Clinical inquiries. Firstor second-generation antihistamines: which are more effective at controlling pruritus? J Fam Pract 2004;53:742.

Hiramanek N: Itch: a symptom of occult disease. Aust Fam Physician 2004;33:495.

Twycross R et al: Itch: scratching more than the surface. QJM 2003;96:7.



  • Itching, chiefly nocturnal, of the anogenital area.

  • Examination is highly variable, ranging from no skin findings to excoriations and inflammation of any degree, including lichenification.

General Considerations

Most cases have no obvious cause, but multiple specific causes have been identified. Anogenital pruritus may be due to intertrigo, psoriasis, lichen simplex chronicus, or seborrheic or contact dermatitis (from soaps, colognes, douches, contraceptives, and perhaps scented toilet tissue), or it may be due to irritating secretions, as in diarrhea, leukorrhea, or trichomoniasis, or to local disease (candidiasis, dermatophytosis, erythrasma). Oxyuriasis (pinworm) is a rare cause in adults. Lichen sclerosus may at times be the cause. Erythrasma is easily diagnosed by demonstration of coral-red fluorescence with Wood's light; it is easily cured with erythromycin orally and topically.

Uncleanliness may be at fault. In pruritus ani, hemorrhoids are often found, and leakage of mucus and bacteria from the distal rectum onto the perianal skin may be important in cases in which no other skin abnormality is found.

Many women experience pruritus vulvae. In women, pruritus ani by itself is rare, and pruritus vulvae does not usually involve the anal area, though anal itching will usually spread to the vulva. In men, pruritus of the scrotum is most commonly seen in the absence of pruritus ani. When all possible known causes have been ruled out, the condition is diagnosed as idiopathic or essential pruritus—by no means rare.

Clinical Findings


The only symptom is itching, which is chiefly nocturnal. Physical findings are usually not present, but there may be erythema, fissuring, maceration, lichenification, excoriations, or changes suggestive of candidiasis or tinea.


Urinalysis and blood glucose testing may lead to a diagnosis of diabetes mellitus. Microscopic examination or culture of tissue scrapings may reveal yeasts or fungi. Stool examination may show pinworms.

Differential Diagnosis

The etiologic differential diagnosis consists of candida infection, parasitosis, local irritation from contact with drugs and irritants, and other primary skin disorders of the genital area such as psoriasis, seborrhea, intertrigo, or lichen sclerosus et atrophicus.


Instruct the patient in proper anogenital hygiene after treating systemic or local conditions.



Treating constipation, preferably with high-fiber management (psyllium), may help. Instruct the patient to use very soft or moistened tissue or cotton after bowel movements


and to clean the perianal area thoroughly with cool water if possible. Women should use similar precautions after urinating. Instruct the patient regarding the harmful and pruritus-inducing effects of scratching.


Pramoxine cream or lotion or hydrocortisone-pramoxine (Pramosone), 1% or 2.5% cream, lotion, or ointment, is helpful in managing pruritus in the anogenital area. The ointment or cream should be applied after a bowel movement. Potent fluorinated topical corticosteroids may lead to atrophy and striae if used for more than a few days and should in general be avoided. This includes combinations with antifungals. The use of strong corticosteroids on the scrotum may lead to persistent severe burning upon withdrawal of the drug. Soaks with aluminum subacetate solution, 1:20, are of value if the area is acutely inflamed and oozing. Underclothing should be changed daily. Balneol Perianal Cleansing Lotion or Tucks premoistened pads, ointment, or cream (all Tucks preparations contain witch hazel) may be very useful for pruritus ani. Squamous cell carcinoma of the anus and extramammary Paget's disease are rare causes of genital pruritus.


Although benign, anogenital pruritus may be persistent and recurrent.

Handa Y et al: Squamous cell carcinoma of the anal margin with pruritus ani of long duration. Dermatol Surg 2003;29:108.

Heard S: Pruritus ani. Aust Fam Physician 2004;33:511.

Pfenniger JL et al: Common anorectal conditions: Part I. Symptoms and complaints. Am Fam Physician 2001;63:2391.

Welsh B et al: Vulval itch. Aust Fam Physician 2004;33:505.



  • Generalized very severe itching.

  • Pruritic vesicles and pustules in “runs” or “galleries,” especially on finger webs and the heels of the palms and in wrist creases.

  • Mites, ova, and brown dots of feces visible microscopically.

  • Red papules or nodules on the scrotum and on the penile glans and shaft are pathognomonic.

General Considerations

Scabies is caused by infestation with Sarcoptes scabiei. The infestation usually spares the head and neck (though even these areas may be involved in infants, in the elderly, and in patients with AIDS). Scabies is usually acquired by sleeping with or in the bedding of an infested individual or by other close contact. The entire household may be affected.

Clinical Findings


Itching is almost always present and can be quite severe. The lesions consist of more or less generalized excoriations with small pruritic vesicles, pustules, and “runs” or “burrows” in the web spaces and on the heels of the palms, wrists, elbows, and around the axillae. Often, burrows are found only on the feet, as they have been scratched off in other locations. The burrow appears as a short irregular mark, 2–3 mm long and the width of a hair. Characteristic lesions may occur on the nipples in females and as pruritic papules on the scrotum or penis in males. Pruritic papules may be seen over the buttocks.


The diagnosis should be confirmed by microscopic demonstration of the organism, ova, or feces in a mounted specimen. The success of this procedure depends on choosing the best unexcoriated lesions from interdigital webs, wrists, elbows, or feet. A No. 15 blade is used to scrape the lesion until it is flat. Pinpoint bleeding may result from the scraping. The mite, ova, and feces can be seen under the light microscope.

Differential Diagnosis

Scabies must be distinguished from the various forms of pediculosis and from other causes of pruritus.

Treatment & Prognosis

Treatment is aimed at killing scabies mites and controlling the dermatitis, which can persist for months after effective eradication of the mites. Bedding and clothing should be laundered or cleaned or set aside for 14 days in plastic bags. If secondary pyoderma is present, it is treated with systemic antibiotics. Unless treatment is aimed at all infected persons in a family or institutionalized group, reinfestations will probably occur.

Permethrin 5% cream is highly effective and safe in the management of scabies. Treatment consists of a single application for 8–12 hours. It may be repeated in 1 week. The drug has been used safely in infants aged 2 months to 5 years and is the treatment of choice in children. An alternative drug is crotamiton cream or lotion, which may be applied nightly for 4 nights. It is far less effective if used for only 48 hours.

Pregnant patients should be treated only if they have documented scabies themselves. Permethrin 5% cream once for 12 hours—or 5% or 6% sulfur in petrolatum applied nightly for 3 nights from the collarbones down—may be used.


Patients will continue to itch for several weeks after treatment. Use of triamcinolone 0.1% cream will help resolve the dermatitis. Scabies in nursing home patients, institutionalized or mentally impaired (especially Down's syndrome) patients, and AIDS patients may be much more difficult to treat.

Most failures in normal persons are related to incorrect use or incomplete treatment of the housing unit. In these cases, repeat treatment with permethrin once weekly for 2 weeks, with reeducation regarding the method and extent of application, is suggested. In immunocompetent individuals, ivermectin in a dose of 200 mcg/kg is effective in about 75% of cases with a single dose and 95% of cases with two doses 2 weeks apart. In immunosuppressed hosts and those with crusted (hyperkeratotic) scabies, multiple doses of ivermectin (every 2 weeks for two or three doses) plus topical therapy with permethrin once or twice weekly may be effective when topical treatment and oral therapy alone fail.

Persistent pruritic postscabietic papules may be treated with midto high-potency corticosteroids or with intralesional triamcinolone acetonide (2.5–5 mg/ mL).

Gimenez Garcia R et al: Scabies in the elderly. J Eur Acad Dermatol Venereol 2004;18:105.



  • Pruritus with excoriation.

  • Nits on hair shafts; lice on skin or clothes.

  • Occasionally, sky-blue macules (maculae ceruleae) on the inner thighs or lower abdomen in pubic louse infestation.

General Considerations

Pediculosis is a parasitic infestation of the skin of the scalp, trunk, or pubic areas. Body lice usually occur among people who live in overcrowded dwellings with inadequate hygiene facilities. Pubic lice may be acquired by sexual transmission. Head lice may be transmitted by shared use of hats or combs and are epidemic among children of all socioeconomic classes in elementary schools. Head lice are very uncommon among black children. Adults contacting children with head lice frequently acquire the infestation.

There are three different varieties: (1) pediculosis pubis, caused by Pthirus pubis (pubic louse, “crabs”); (2) pediculosis corporis, caused by Pediculus humanus var corporis (body louse); and (3) pediculosis capitis, caused by Pediculus humanus var capitis (head louse).

Head and body lice are similar in appearance and are 3–4 mm long. The body louse can seldom be found on the body, because the insect comes onto the skin only to feed and must be looked for in the seams of the clothing. Trench fever, relapsing fever, and typhus are transmitted by the body louse in countries where those diseases are endemic.

Clinical Findings

Itching may be very intense in body louse infestations, and scratching may result in deep excoriations, especially over the upper shoulders, posterior flanks, and neck. In some cases, only itching is present, with few excoriations seen. Pyoderma may be the presenting sign in any of these infestations. Head lice can be found on the scalp or may be manifested as small nits resembling pussy willow buds on the scalp hairs close to the skin. They are easiest to see above the ears and at the nape of the neck. Pubic louse infestations are occasionally generalized, particularly in hairy individuals; the lice may even be found on the eyelashes and in the scalp.

Differential Diagnosis

Head louse infestation must be distinguished from seborrheic dermatitis, body louse infestation from scabies, and pubic louse infestation from anogenital pruritus and eczema.


Body lice are treated by disposing of the infested clothing. For pubic lice, permethrin rinse 1% for 10 minutes and permethrin cream 5% applied for 8 hours are effective. Sexual contacts should be treated. Clothes and bedclothes should be washed and dried at high temperature if possible.

Permethrin 1% cream rinse (Nix) is a topical overthe-counter pediculicide and ovicide and is the treatment of choice for head lice. It is applied to the scalp and hair and left on for 30 minutes to 8 hours before being rinsed off. Treatment should be repeated in 1 week. Five percent permethrin lotion may be used in refractory cases. Permethrin resistance of head lice is common. Malathion lotion 1% (Ovide) is very effective, but it is highly volatile and flammable, so application must be done in a well-ventilated room or out of doors. For involvement of eyelashes, petrolatum is applied thickly twice daily for 8 days, and remaining nits are then plucked off. Adults with head lice virtually always acquire their infestation from elementary schoolaged children, so a source of infection must always be sought. Head lice are extremely difficult to eradicate in the epidemic setting, probably because the currently available pediculicides are not uniformly ovicidal when applied as directed.

Dodd CS: Interventions for treating headlice. Cochrane Database Syst Rev 2001;(3):CD001165.


Huynh TH et al: Scabies and pediculosis. Dermatol Clin 2004;22:7.

Thappa DM et al: Phthiriasis palpebrarum. Postgrad Med J 2003;79:102.



  • Localized rash with pruritus.

  • Furuncle-like lesions containing live arthropods.

  • Tender erythematous patches that migrate (“larva migrans”).

  • Generalized urticaria or erythema multiforme in some patients.

General Considerations

Some arthropods (eg, mosquitoes and biting flies) are readily detected as they bite. Many others are not, eg, because they are too small, because there is no immediate reaction, or because they bite during sleep. Reactions may be delayed for hours; many are allergic. Patients are most apt to consult a clinician when the lesions are multiple and pruritus is intense.

Many persons will react severely only to their earliest contacts with an arthropod, thus presenting pruritic lesions when traveling, moving into new quarters, etc. Body lice, fleas, bedbugs, and mosquitoes should be considered. Spiders are often incorrectly believed to be the source of bites; they rarely attack humans, though the brown spider (Loxosceles laeta, Loxosceles reclusa) may cause severe necrotic reactions and death due to intravascular hemolysis, and the black widow spider (Latrodectus mactans) may cause severe systemic symptoms and death. (See also Chapter 39.)

In addition to arthropod bites, the most common lesions are venomous stings (wasps, hornets, bees, ants, scorpions) or bites (centipedes), furuncle-like lesions due to fly maggots or sand fleas in the skin, and a linear creeping eruption due to a migrating larva.

Clinical Findings

The diagnosis may be difficult when the patient has not noticed the initial attack but suffers a delayed reaction. Individual bites are often in clusters and tend to occur either on exposed parts (eg, midges and gnats) or under clothing, especially around the waist or at flexures (eg, small mites or insects in bedding or clothing). The reaction is often delayed for 1–24 hours or more. Pruritus is almost always present and may be all but intolerable once the patient starts to scratch. Secondary infection may follow scratching. Urticarial wheals are common. Papules may become vesicular.

The diagnosis is aided by searching for exposure to arthropods and by considering the patient's occupation and recent activities.

The principal arthropods are as follows:

1. Fleas

Fleas are bloodsucking ectoparasites that feed on dogs, cats, humans, and other species. Flea saliva produces papular urticaria in sensitized individuals. To break the life cycle of the flea, one must treat the home and pets, using quick-kill insecticides, residual insecticides, and a growth regulator.

2. Bedbugs

In crevices of beds or furniture; bites tend to occur in lines or clusters. Papular urticaria is a characteristic lesion of bedbug (Cimex lectularius) bites. The closely related kissing bug has a painful bite.

3. Ticks

Usually picked up by brushing against low vegetation. Ticks may transmit Rocky Mountain spotted fever, Lyme disease, relapsing fever, and ehrlichiosis.

4. Chiggers or red bugs

These are larvae of trombiculid mites. A few species confined to particular regions and locally recognized habitats (eg, berry patches, woodland edges, lawns, brush turkey mounds in Australia, poultry farms) attack humans, often around the waist, on the ankles, or in flexures, raising intensely itching erythematous papules after a delay of many hours. The red chiggers may sometimes be seen in the center of papules that have not yet been scratched.

5. Bird and rodent mites

Larger than chiggers, bird mites infest pigeon lofts or nests of birds in eaves. Bites are multiple anywhere on the body. Room air conditioning units may suck in bird mites and infest the inhabitants of the room. Rodent mites from mice or rats may cause similar effects. Pet gerbils may be infested with bird mites. The diagnosis of bird mites or rodent mites may easily be overlooked.

6. Mites in stored products

These are white and almost invisible and infest products such as copra, vanilla pods, sugar, straw, cottonseeds, and cereals. Persons who handle these products may be attacked, especially on the hands and forearms and sometimes on the feet. Infested bedding may occasionally lead to generalized dermatitis.

7. Caterpillars of moths with urticating hairs

The hairs are blown from cocoons or carried by emergent moths, causing severe and often seasonally recurrent outbreaks after mass emergence. The gypsy moth is a cause in the eastern United States.

8. Tungiasis

Tungiasis is due to the burrowing flea known as Tunga penetrans and is found in Africa, the West Indies, and South and Central America. The female burrows under the skin, sucks blood, swells to 0.5 cm, and then ejects her eggs onto the ground. Ulceration, lymphangitis, gangrene, and septicemia may result, in some cases with lethal effect. Ethyl chloride spray will kill the insect when applied to the lesion, and disinfestation may be accomplished with insecticide applied to the terrain. Simple surgical excision is usually performed.


Differential Diagnosis

Arthropods should be considered in the differential diagnosis of skin lesions showing any of the above symptoms.


Arthropod infestations are best prevented by avoidance of contaminated areas, personal cleanliness, and disinfection of clothing, bedclothes, and furniture as indicated. Chiggers, bedbugs, and mites can be killed by permethrin applied to the head and clothing. (It is not necessary to remove clothing.)


Living arthropods should be removed carefully with tweezers after application of alcohol and preserved in alcohol for identification. In endemic Rocky Mountain spotted fever areas, ticks should not be removed with the bare fingers.

Corticosteroid lotions or creams are helpful. Topical antibiotics may be applied if secondary infection is suspected. Localized persistent lesions may be treated with intralesional corticosteroids.

Stings produced by many arthropods may be alleviated by applying papain powder (Adolph's Meat Tenderizer) mixed with water, or aluminum chloride hexahydrate (Xerac AC).

Extracts from venom sacs of bees, wasps, yellow jackets, and hornets are available for immunotherapy of patients at risk for anaphylaxis.

Creel NB et al: Pet hamsters as a source of rat mite dermatitis. Cutis 2003;71:457.

Diba VC et al: Cutaneous larva migrans acquired in Britain. Clin Exp Dermatol 2004;29:555.

Whyte AS et al: Bats in the belfry, bugs in the bed? Lancet 2001;357:604.




  • Painful red nodules without ulceration on anterior aspects of legs.

  • Slow regression over several weeks to resemble contusions.

  • Women are predominantly affected by a ratio of 10:1 over men.

  • Some cases associated with infection or drug sensitivity.

General Considerations

Erythema nodosum is a symptom complex characterized by tender, erythematous nodules that appear most commonly on the extensor surfaces of the lower legs. It usually lasts about 6 weeks and may recur. The disease may be associated with various infections—streptococcosis, primary coccidioidomycosis, other deep fungal infections, tuberculosis, Yersinia pseudotuberculosis and Yersinia enterocolitica infection, or syphilis. It may accompany sarcoidosis and inflammatory bowel disease. Erythema nodosum may be associated with pregnancy or with use of oral contraceptives or other medication.

Clinical Findings


The swellings are exquisitely tender and may be preceded by fever, malaise, and arthralgia. They are most often located on the anterior surfaces of the legs below the knees but may occur (rarely) on the arms, trunk, and face. The lesions, 1–10 cm in diameter, are at first pink to red; with regression, all the various hues seen in a contusion can be observed.


The histologic finding of septal panniculitis is characteristic of erythema nodosum. Evaluation of patients presenting with acute erythema nodosum should include a careful history (including drug exposures) and physical examination for prior upper respiratory infection or diarrheal illness, symptoms of any deep fungal infection endemic to the area, a chest x-ray, a PPD, and two consecutive ASO/DNAseB titers at 2to 4week intervals. If no underlying cause is found, only a small percentage of patients will go on to develop a significant underlying illness (usually sarcoidosis) over the next year.

Differential Diagnosis

Erythema induratum from tuberculosis is seen on the posterior surfaces of the legs and may ulcerate. Lupus panniculitis presents as tender nodules on the buttocks and posterior arms that heal with depressed scars. Polyarteritis nodosa is less inflammatory, and the subcutaneous nodules are often associated with a fixed livedo. In the late stages, erythema nodosum must be distinguished from simple bruises and contusions.


First, the underlying cause should be identified and treated. Primary therapy is with NSAIDs in usual doses. Saturated solution of potassium iodide, 5–15 drops three times daily, results in prompt involution in many cases. Side effects of potassium iodide include salivation, swelling of salivary glands, and headache. Complete bed rest may be advisable if the lesions


are painful. Systemic therapy directed against the lesions themselves may include corticosteroid therapy (see Chapter 26) unless contraindicated by associated infection.


The lesions usually disappear after about 6 weeks, but they may recur.

Katugampola RP et al: Intestinal bypass syndrome presenting as erythema nodosum. Clin Exp Dermatol 2004;29:261.

Mert A et al: Erythema nodosum: an experience of 10 years. Scand J Infect Dis 2004;36:424.



  • Extremely painful inflammatory swelling based on a hair follicle that forms an abscess.

  • Predisposing condition (diabetes mellitus, HIV disease, injection drug use) sometimes present.

  • Coagulase-positive Staphylococcus aureus is the causative organism.

General Considerations

A furuncle (boil) is a deep-seated infection (abscess) involving the entire hair follicle and adjacent subcutaneous tissue. The most common sites of occurrence are the hairy parts exposed to irritation and friction, pressure, or moisture. Because the lesions are autoinoculable, they are often multiple. Diabetes mellitus (especially if using insulin injections), injection drug use, allergy injections, and HIV disease all increase the risk of staphylococcal infections by increasing the rate of nasal carriage.

A carbuncle consists of several furuncles developing in adjoining hair follicles and coalescing to form a conglomerate, deeply situated mass with multiple drainage points.

Clinical Findings


Pain and tenderness may be prominent. The abscess is either rounded or conical. It gradually enlarges, becomes fluctuant, and then softens and opens spontaneously after a few days to 1–2 weeks to discharge a core of necrotic tissue and pus. The inflammation occasionally subsides before necrosis occurs. Infection of the soft tissue around the nails (paronychia) may be due to staphylococci when it is acute or candida when chronic.


There may be slight leukocytosis, but a white blood cell count is rarely required. Pus should be cultured to rule out MRSA or other bacteria. Culture of the anterior nares may identify chronic staphylococcal carriage in cases of recurrent cutaneous infection.

Differential Diagnosis

The most common entity in the differential is an inflamed epidermal inclusion cyst that suddenly becomes red, tender, and expands greatly in size over one to a few days. The history of a prior cyst in the same location, the presence of a clearly visible cyst orifice, and the extrusion of malodorous cheesy rather than purulent material helps in the diagnosis. Tinea profunda (deep dermatophyte infection of the hair follicle) may simulate recurrent furunculosis. Furuncle is also to be distinguished from deep mycotic infections, such as sporotrichosis (often in gardeners); from other bacterial infections, such as anthrax and tularemia (rare); from atypical mycobacterial infections; and from acne cysts. Hidradenitis suppurativa presents with recurrent tender sterile abscesses in the axillae and groin, on the buttocks, or below the breasts. The presence of old scars or sinus tracts plus negative cultures suggests this diagnosis.


Serious and sometimes fatal complications of staphylococcal infection such as septicemia can occur.



Incision and drainage is recommended for all loculated suppurations and is the mainstay of therapy. Systemic antibiotics are indicated (chosen on the basis of cultures and sensitivity tests if possible). Sodium dicloxacillin or cephalexin, 1 g daily in divided doses by mouth for 10 days, is usually effective. Doxycycline 100 mg twice daily, trimethoprim-sulfamethoxazole DS one tablet twice daily, and clindamycin 150–300 mg twice daily are effective in treating MRSA. Recurrent furunculosis may be effectively treated with a combination of cephalexin, 250–500 mg four times daily for 2–4 weeks, and rifampin, 300 mg twice daily for 5 days during this period. Chronic clindamycin, 150–300 mg daily for 1–2 months, may also cure recurrent furunculosis. Family members and intimate contacts may need evaluation for staphylococcal carrier state and perhaps concomitant treatment. Applications of topical 2% mupirocin to the nares, axillae, and anogenital areas twice daily for 5 days may eliminate the staphylococcal carrier state.


Immobilize the part and avoid overmanipulation of inflamed areas. Use moist heat to help larger lesions


“localize.” Use surgical incision and debridement after the lesions are “mature.” To incise and drain an acute staphylococcal paronychia, insert a flat metal spatula or sharpened hardwood stick into the nail fold where it adjoins the nail. This will release pus from a mature lesion. Inflamed epidermal cysts may be treated in the initial stages with intralesional injections of triamcinolone acetonide into the borders of the lesions plus drainage of fluctuant lesions results in rapid resolution and reduction of pain.


Recurrent crops may harass the patient for months or years.

Baggett HC et al: Community-onset methicillin-resistant Staphylococcus aureus associated with antibiotic use and the cytotoxin Panton-Valentin leukocidin during a furunculosis outbreak in rural Alaska. J Infect Dis 2004;189: 1565.

Gira AK et al: Furunculosis due to Mycobacterium mageritense associated with footbaths at a nail salon. J Clin Microbiol 2004;42:1813.

Laube S et al: Bacterial skin infections in the elderly: diagnosis and treatment. Drugs Aging 2002;19:331.

Stulberg DL et al: Common bacterial skin infections. Am Fam Physician 2002;66:119.

Winthrop KL et al: The clinical management and outcome of nail salon-acquired Mycobacterium fortuitum skin infection. Clin Infect Dis 2004;38:38.



  • Firm dermal papule or nodule.

  • Overlying black comedone or “punctum.”

  • Expressable foul-smelling cheesy material.

  • May become red and drain, mimicking an abscess.

General Considerations

Epidermal inclusion cysts (EICs) are common, benign growths of the upper portion of the hair follicle. They are common in Gardner's syndrome and may be the first stigmata of the condition.

Epidermal inclusion cysts favor the face and trunk and may complicate nodulocystic acne vulgaris. Individual lesions range in size from 0.3 cm to several centimeters. An overlying pore or punctum is characteristic. Lateral pressure may lead to extrusion of a foul-smelling, cheesy material.

Differential Diagnosis

EICs are distinguished from lipomas by being more superficial (in the dermis not the subcutaneous fat) and by their overlying punctum. Many other benign and malignant tumors may superficially resemble EICs, but all lack the punctum.


EICs may rupture, creating an acute inflammatory nodule very similar to an abscess. Cultures of the expressed material will be sterile.


Treatment is not required if asymptomatic. Inflamed lesions may be treated with incision and drainage or intralesional triamcinolone acetomide 5–10 mg/mL. For large, symptomatic cysts, surgical excision is curative.



  • Painful or pruritic erythema, edema, or vesiculation on sun-exposed surfaces: the face, neck, hands, and “V” of the chest.

  • Inner upper eyelids spared, as is the area under the chin.

General Considerations

Photodermatitis is an acute or chronic skin reaction due to hypersensitivity to sunlight or other sources of radiation, photosensitization of the skin by certain drugs, or idiosyncrasy to actinic light as seen in some constitutional disorders including the porphyrias and many hereditary disorders (phenylketonuria, xeroderma pigmentosum, and others). Contact photosensitivity may occur with perfumes, antiseptics, and other chemicals.

Photodermatitis is manifested most commonly as phototoxicity—a tendency for the individual to sunburn more easily than expected—or, as photoallergy, a true immunologic reaction that often presents with dermatitis.

Clinical Findings


The acute inflammatory skin reaction, if severe enough, is accompanied by pain, fever, gastrointestinal symptoms, malaise, and even prostration, but this is very rare. Signs include erythema, edema, and possibly vesiculation


and oozing on exposed surfaces. Peeling of the epidermis and pigmentary changes often result. The key to diagnosis is localization of the rash to photoexposed areas, though these eruptions may become generalized with time to involve even photoprotected areas. The lower lip is commonly involved in hereditary polymorphous light eruption, a disorder seen in persons of Native American descent.


Blood and urine tests are not helpful in diagnosis unless porphyria cutanea tarda is suggested by the presence of blistering, scarring, milia (white cysts 1–2 mm in diameter) and skin fragility of the dorsal hands, and facial hypertrichosis. Testing for photosensitivity may define the wavelengths of light triggering the reaction. This is critical in determining the form of photoprotection recommended.

Differential Diagnosis

The differential diagnosis is long. If a clear history of the use of a topical or systemic photosensitizer is not available and if the eruption is persistent, then a workup including biopsy and light testing may be required. Photodermatitis must be differentiated from contact dermatitis that may develop from one of the many substances in suntan lotions and oils, as these may often have a similar distribution. Sensitivity to actinic rays may also be part of a more serious condition such as porphyria cutanea tarda or lupus erythematosus. These disorders are diagnosed by appropriate blood or urine tests. Phenothiazines, quinine or quinidine, griseofulvin, sulfonylureas, NSAIDs, and antibiotics (eg, some tetracyclines, quinolone, trimethoprim-sulfamethoxazole) may photosensitize the skin. Polymorphous light eruption is a very common idiopathic photodermatitis that affects both sexes equally and often has its onset in the third to fourth decades except in Native Americans and Latinos, in whom it commonly presents in childhood. Polymorphous light eruption is chronic in nature. Transitory periods of spontaneous remission do occur. The action spectrum usually lies in the short (below 320 nm) ultraviolet wavelengths but may also extend into the long ultraviolet wavelengths (320–400 nm).


Some individuals continue to be chronic light reactors even when they apparently are no longer exposed to photosensitizing drugs.


While sunscreens are useful agents in general and should be used by persons with photosensitivity, patients may react to such low amounts of energy that sunscreens alone may not be sufficient. Sunscreens with an SPF of 30–50, usually containing avobenzone (Parasol 1789), titanium dioxide, and micronized zinc oxide, are especially useful in patients with photoallergic dermatitis.



Drugs should be suspected in cases of photoallergy even if the particular medication (such as hydrochlorothiazide) has been used for months.


When the eruption is vesicular or weepy, treatment is similar to that of any acute dermatitis, using cooling and soothing wet dressing.

Sunscreens should be used as described above. Midpotency to high-potency topical corticosteroids are of limited benefit in phototoxic reactions but may help in polymorphous light eruption and photoallergic reactions. Since the face is often involved, close monitoring is necessary to avoid side effects of potent corticosteroids.


Aspirin may have some value for fever and pain of acute sunburn, as prostaglandins appear to play a pathogenetic role in the early erythema. Systemic corticosteroids in doses as described for acute contact dermatitis may be required for severe photosensitivity reactions. Otherwise, different photodermatoses may be treated in specific ways.

Patients with severe photodermatitis may require immunosuppressives, such as azathioprine, in the range of 50–150 mg/d; or cyclosporine, 3–5 mg/kg/d.


The most common phototoxic sunburn reactions are usually benign and self-limiting except when the burn is severe or when it occurs as an associated finding in a more serious disorder. Polymorphous light eruption and some cases of photoallergy can persist for years.

Bilu D et al: Clinical and epidemiologic characterization of photosensitivity in HIV-positive individuals. Photodermatol Photoimmunol Photomed 2004;20:175.

Brunner KL et al: Extreme photosensitivity. Mayo Clin Proc 2004;79:1316.

Dolan CK et al: Pseudoporphyria as a result of voriconazole use: a case report. Int J Dermatol 2004;43:768.

Morison WL: Clinical practice. Photosensitivity. N Engl J Med 2004;350:1111.


DECUBITUS ULCERS (Bedsores, Pressure Sores)

Bedsores (pressure sores) are a special type of ulcer caused by impaired blood supply and tissue nutrition resulting from prolonged pressure over bony or cartilaginous prominences. The skin overlying the sacrum and hips is most commonly involved, but bedsores may also be seen over the occiput, ears, elbows, heels,


and ankles. They occur most readily in aged, paralyzed, debilitated, and unconscious patients. Lowgrade infection may occur as a complication.

Table 6-3. Staging system for classifying pressure ulcers.

Grade Description
1 Intact skin. Fixed erythema (pink, red or mottled) after pressure is relieved.
2 Loss of epidermis or dermis. Resembles blister, abrasion, or shallow crater. Necrotic tissue may overlie ulcer.
3 Ulceration through the epidermis and dermis with damage to the underlying subcutaneous fat. Ulcer may extend to the fascia.
4 Full thickness skin loss with extension of the ulcer to bone, muscle, tendon, or joint.
5 Closed cavity communicating through a small sinus.

Treatment costs for a pressure ulcer exceed $20,000 in most cases and hospital stay extensions due to severe pressure ulcers may cost in excess of $200,000. Standard staging systems are used to classify pressure ulcers (Table 6-3). In all non-healing ulcerations, there is a concern for underlying osteomyelitis. This is especially true for grade 3 to 5 ulcers.

Differential Diagnosis

Herpes simplex virus should be suspected in ulcers in immunocompromised patients, particularly if there is a scalloped border, representing the erosions of herpetic vesicles. Rarely, ulcerated lesions in the perianal area represent actual skin cancers. Rapidly expanding ulcers may also represent pyoderma gangrenosum associated with inflammatory bowel disease. Ecthyma gangrenosum is an ulcerating lesion, commonly due to Pseudomonas, and observed in neutropenic patients. All ulcerative lesions should be biopsied and cultured if suspicious or if they do not heal properly.


The most important element of treatment of pressure ulcers is prevention. Good nursing care, good nutrition, and maintenance of skin hygiene are important preventive measures. The skin and the bed linens should be kept clean and dry. Bedfast, paralyzed, moribund, listless, or incontinent patients who are candidates for the development of decubiti must be turned frequently (at least every hour) and must be examined at pressure points for the appearance of small areas of redness and tenderness. Written schedules can be very helpful. Water-filled mattresses, rubber pillows, alternating-pressure mattresses, and thick papillated foam pads are useful in prevention and in the treatment of lesions. “Donut” devices should not be used. Avoidance of smoking and a “healthy lifestyle” are associated with avoiding pressure ulcers in spinal cord injury patients.


A large number of treatments and protocols exist for management of decubiti. Early lesions should be treated with topical antibiotic powders and adhesive absorbent bandage (Gelfoam). Once clean, they may be treated with hydrocolloid dressings such as DuoDerm. Established lesions require surgery for debridement, cleansing, and dressing. A spongy foam pad placed under the patient may work best in some cases. It must be laundered often. In general, topical antiseptics are not recommended. Systemic antibiotics are required for deep infections.

Brem H et al: Protocol for the successful treatment of pressure ulcers. Am J Surg 2004;188:9.

Krause JS et al: Patterns of recurrent pressure ulcers after spinal cord injury: identification of risk and protective factors 5 or more years after onset. Arch Phys Med Rehabil 2004;85: 1257.



  • Past history of varicosities, thrombophlebitis, or postphlebitic syndrome.

  • Irregular ulceration, often on the medial aspect of the lower legs above the malleolus.

  • Edema of the legs, varicosities, hyperpigmentation, and red and scaly areas (stasis dermatitis) and scars from old ulcers support the diagnosis.

General Considerations

Patients at risk may have a history of venous insufficiency, either with obvious varicosities or with a past history of thrombophlebitis, or with immobility of the calf muscle group (paraplegics, etc). Red, pruritic patches of stasis dermatitis often precede ulceration. Because venous insufficiency is the most common cause of lower leg ulceration, testing of venous competence is still a required part of the evaluation even when no changes of venous insufficiency are present.

Clinical Findings


Classically, chronic edema is followed by a dermatitis, which is often pruritic. These changes are followed by hyperpigmentation, skin breakdown, and eventually sclerosis of the skin of the lower leg. The ulcer base


may be clean, but it often has a yellow fibrin eschar that frequently requires surgical treatment. Ulcers that appear on the feet, toes, or above the knees should be approached with other diagnoses in mind.


Thorough evaluation of the patient's vascular system (including measurement of the ankle/brachial index) is essential. Doppler and light rheography examinations as office procedures are usually sufficient (except in the diabetic) to elucidate the cause of most vascular cases of lower leg ulceration.

Differential Diagnosis

The differential includes vasculitis, pyoderma gangrenosum, arterial ulcerations, infection, trauma, skin cancer, arachnid bites, and sickle cell anemia. When the diagnosis is in doubt, a punch biopsy from the border (not base) of the lesion may be helpful.


Compression stockings to reduce edema are the most important means of prevention. Compression should achieve a pressure of 30 mm Hg below the knee and 40 mm Hg at the ankle. The stockings should not be used in patients with arterial insufficiency with an ankle-brachial pressure index less than 0.7. Pneumatic sequential compression devices may be of great benefit when edema is refractory to standard compression dressings.



Institution of compression therapy is begun after cleaning of the ulcer with saline or cleansers such as Saf-Clens. A curette or small scissors can be used to remove the yellow fibrin eschar; local anesthesia may be used if the areas are very tender.

The ulcer is treated with metronidazole gel to reduce bacterial growth and odor. Any red dermatitic skin is treated with a mediumto high-potency corticosteroid ointment. The ulcer is then covered with an occlusive hydroactive dressing (DuoDerm or Cutinova) or a polyurethane foam (Allevyn) followed by an Unna zinc paste boot. This is changed weekly. The ulcer should begin to heal within weeks, and healing should be complete within 4–6 months. If the patient is diabetic, becaplermin (Regranex) may be applied to the ulcer along with good local treatment in those ulcers which are not becoming smaller or developing a granulating base. Some ulcerations require grafting. Fullor split-thickness grafts often do not take, and pinch grafts (small shaves of skin laid onto the bed) may be more effective. Cultured epidermal cell grafts may accelerate wound healing, but they are very expensive. They should be considered in refractory ulcers, especially those that have not healed after a year or more of conservative therapy.


Pentoxifylline, 400 mg three times daily administered with compression, is beneficial in accelerating healing of leg ulcers. Zinc supplementation is occasionally beneficial in patients with low serum zinc levels. If cellulitis accompanies the ulcer, systemic antibiotics are recommended: dicloxacillin, 250 mg orally four times a day, or levofloxacin, 500 mg once daily for 1–2 weeks is usually adequate. If infection persists, an underlying osteomyelitis should be sought.


The combination of compression stockings and newer dressings enables venous stasis ulcers to heal within months. Topical growth factors, antibiotics, debriding agents, and xenografts and autografts have been shown to be effective in recalcitrant cases. Ongoing control of edema is essential to prevent recurrent ulceration.

de Araujo T et al: Managing the patient with venous ulcers. Ann Intern Med 2003;138:326.



Although the color of skin may be altered by many diseases and agents, the vast majority of patients have either an increase or decrease in pigment secondary to some inflammatory disease such as acne or atopic dermatitis.

Other pigmentary disorders include those resulting from exposure to exogenous pigments such as carotenemia, argyria, deposition of other metals (such as gold when given long-term for rheumatoid arthritis), and tattooing. Other endogenous pigmentary disorders are attributable to metabolic substances—including hemosiderin (iron)—in purpuric processes; or to homogentisic acid in ochronosis; bile pigments; and carotenes.


First, determine whether the disorder is hyperpigmentation or hypopigmentation, ie, an increase or decrease in normal skin colors. Each may be considered to be primary or to be secondary to other disorders.



1. Hyperpigmentation

The disorders in this category are nevoid, congenital or acquired, and include pigmented nevi, ephelides (juvenile freckles), and lentigines (senile freckles). Hyperpigmentation occurs also in arsenical melanosis or in association with Addison's disease (due to lack of the inhibitory influence of cortisol on the production of melanocyte-stimulating hormone by the pituitary gland). Axillary freckling and caf au lait spots may be seen in neurofibromatosis. Melasma (chloasma) occurs as patterned hyperpigmentation of the face, usually as a direct effect of estrogens. It occurs not only during pregnancy but also in 30–50% of women taking oral contraceptives, and rarely in men. One report suggests that such men have low testosterone and elevated luteinizing hormone levels.

2. Hypopigmentation and depigmentation

The disorders in this category are vitiligo, albinism, and piebaldism. In vitiligo, pigment cells (melanocytes) are destroyed. Vitiligo, present in approximately 1% of the population, may be associated with hyperthyroidism and hypothyroidism, pernicious anemia, diabetes mellitus, and Addison's disease. Albinism represents a number of different genetically determined traits, with different phenotypes. These often affect the eye and vision. Piebaldism, a localized hypomelanosis manifested by a white forelock, is an autosomal dominant trait that in some cases may be associated with neurologic abnormalities. Hypopigmented ash leaf spots may be seen in tuberous sclerosis. Hypopigmented halos are common around nevi and may occur around melanomas.


Any damage to the skin (irritation, allergy, infection, excoriation, burns, or dermatologic therapy such as chemical peels and freezing with liquid nitrogen) may result in hyperpigmentation or hypopigmentation. Several disorders of clinical importance are described below.

1. Hyperpigmentation

The most common type of secondary hyperpigmentation occurs after another dermatologic condition, such as acne, and is most commonly seen in dark-skinned persons. It is called postinflammatory hyperpigmentation.

Berloque hyperpigmentation is the pigmentation due to phototoxicity from chemicals in the rinds of limes and other citrus fruits and to celery. Pigmentation may be produced by certain drugs, eg, chloroquine, chlorpromazine, minocycline, and amiodarone. Irritation from benzoyl peroxide and tretinoin can result in hyperpigmentation, as may topical fluorouracil. Fixed drug eruptions to phenolphthalein in laxatives, to trimethoprim-sulfamethoxazole, to NSAIDs, and to tetracyclines, for example, are further causes.

2. Hypopigmentation

Leukoderma is a disorder that may complicate atopic dermatitis, lichen planus, psoriasis, DLE, and lichen simplex chronicus. Practitioners must exercise special care in using liquid nitrogen on any patient with olive or darker complexions, since doing so may result in hypopigmentation or depigmentation, at times permanent. Intralesional or intra-articular injections of high concentrations of corticosteroids may also cause localized temporary hypopigmentation.

Differential Diagnosis

One must distinguish true lack of pigment from pseudoachromia, such as occurs in tinea versicolor, pityriasis simplex, and seborrheic dermatitis. The evaluation of pigmentary disorders in whites is helped by Wood's light, which accentuates epidermal pigmentation and highlights hypopigmentation.


Actinic keratoses and skin cancers are more likely to develop in persons with vitiligo and albinism. There may be severe emotional trauma in extensive vitiligo and other types of hypopigmentation and hyperpigmentation, particularly when they occur in naturally dark-skinned persons.

Treatment & Prognosis


Therapeutic bleaching preparations generally contain hydroquinone. Hydroquinone has occasionally caused unexpected hypopigmentation, hyperpigmentation, or even secondary ochronosis and pigmented milia, particularly with prolonged use.

The role of exposure to ultraviolet light cannot be overstressed as a factor promoting or contributing to most disorders of hyperpigmentation, and such exposure should be minimized. Melasma, ephelides, and postinflammatory hyperpigmentation may be treated with varying success with 3–4% hydroquinone cream, gel, or solution and a sunscreen containing UVA photoprotectants (Avobenzone, zinc oxide, titanium dioxide). Tretinoin cream, 0.025–0.05%, may be added. Superficial melasma responds well, but if there is predominantly dermal deposition of pigment (does not enhance with Wood's light), the prognosis is poor. Response to therapy takes months and requires avoidance of sunlight. Hyperpigmentation often recurs after treatment if the skin is exposed to ultraviolet light. Solar lentigines respond to liquid nitrogen application. Tretinoin, 0.1% cream and tazarotene 0.1% used over 10 months, will fade solar lentigines (liver spots), hyperpigmented facial macules in Asians, and postinflammatory hyperpigmentation in blacks. New laser systems for the removal of epidermal and dermal pigments are available, and referral should be considered for patients whose responses to medical treatment are inadequate.


The pigment dilution is stable in various forms of albinism; spontaneous return of pigment is rare in vitiligo;


in secondary hypopigmentation, repigmentation may occur spontaneously. Cosmetics such as Covermark and Dermablend are highly effective for concealing disfiguring patches. Therapy of vitiligo is long and tedious, and the patient must be strongly motivated. If less than 20% of the skin is involved (most cases), topical tacrolimus 0.1% twice daily is the first-line therapy. A superpotent corticosteroid may also be used, but local skin atrophy from prolonged use may ensue. With 20–25% involvement, narrowband UVB or oral PUVA is best. Severe phototoxic response (sunburn) may occur with oral PUVA. The face and upper chest respond best, and the fingertips and the genital areas do not respond as well to treatment. Years of treatment may be required. Newer techniques of using epidermal autografts and cultured epidermis combined with PUVA therapy give hope for surgical correction of vitiligo.

Czajkowski R: Comparison of melanocytes transplantation methods for the treatment of vitiligo. Dermatol Surg 2004;30: 1400.

Egli F et al: Images in clinical medicine. Vitiligo and pernicious anemia. N Engl J Med 2004;350:2698.

Kullavanijaya P et al: Topical calcipotriene and narrowband ultraviolet B in the treatment of vitiligo. Photodermatol Photoimmunol Photomed 2004;20:248.

Stulberg DL et al: Common hyperpigmentation disorders in adults: Part II. Melanoma, seborrheic keratoses, acanthosis nigricans, melasma diabetic dermopathy, tinea versicolor and postinflammatory hyperpigmentation. Am Fam Physician 2003;68:1963.

Travis LB et al: Successful treatment of vitiligo with 0.1% tacrolimus ointment. Arch Dermatol 2003;139:571.

BALDNESS (Alopecia)

Baldness Due to Scarring

Cicatricial baldness may occur following chemical or physical trauma, lichen planopilaris, bacterial or fungal infections, severe herpes zoster, chronic DLE, scleroderma, and excessive ionizing radiation. The specific cause is often suggested by the history, the distribution of hair loss, and the appearance of the skin, as in LE. Biopsy is useful in the diagnosis of scarring alopecia, but specimens must be taken from the active border and not from the scarred central zone.

Scarring alopecias are irreversible and permanent. It is important to diagnose and treat the scarring process as early in its course as possible.

Baldness Not Due to Scarring

Nonscarring alopecia may occur in association with various systemic diseases such as SLE, secondary syphilis, hyperthyroidism or hypothyroidism, iron deficiency anemia, and pituitary insufficiency. The only treatment necessary is prompt and adequate control of the underlying disorder, in which case hair loss may be reversible.

Androgenetic (pattern) baldness, the most common form of alopecia, is of genetic predetermination. The earliest changes occur at the anterior portions of the calvarium on either side of the “widow's peak” and on the crown (vertex) of the skull. The extent of hair loss is variable and unpredictable. Rogaine Extra Strength, a solution containing 50 mg/mL of minoxidil, is available over the counter. The best results are achieved in persons with recent onset (< 5 years) and smaller areas of alopecia. Approximately 40% of patients treated twice daily for a year will have moderate to dense growth. Finasteride (Propecia), 1 mg orally daily, has similar efficacy and may be additive to minoxidil. As opposed to minoxidil, finasteride is used only in males.

Hair loss or thinning of the hair in women results from the same cause as common baldness in men (androgenetic alopecia) and may be treated with minoxidil (Rogaine). A workup consisting of determination of serum testosterone, DHEAS, iron, total iron binding capacity, thyroid function tests, and a complete blood count will identify most other causes of hair thinning in premenopausal women. Women who complain of thin hair but show little evidence of alopecia need follow-up, because more than 50% of the scalp hair can be lost before the clinician can perceive it.

Telogen effluvium is transitory increase in the number of hairs in the telogen (resting) phase of the hair growth cycle. This may occur spontaneously, may appear at the termination of pregnancy, may be precipitated by “crash dieting,” high fever, stress from surgery or shock, or malnutrition, or may be provoked by hormonal contraceptives. Whatever the cause, telogen effluvium usually has a latent period of 2–4 months. The prognosis is generally good. The condition is diagnosed by the presence of large numbers of hairs with white bulbs coming out upon gentle tugging of the hair. Counts of hairs lost by the patient on combing or shampooing often exceed 150 per day, compared to an average of 70–100. In one study, a major cause of telogen effluvium was found to be iron deficiency, and the hair counts bore a clear relationship to serum iron levels.

Alopecia areata is of unknown cause but is believed to be an immunologic process. Typically, there are patches that are perfectly smooth and without scarring. Tiny hairs 2–3 mm in length, called “exclamation hairs,” may be seen. Telogen hairs are easily dislodged from the periphery of active lesions. The beard, brows, and lashes may be involved. Involvement may extend to all of the scalp hair (alopecia totalis) or to all scalp and body hair (alopecia universalis). Severe forms may be treated by systemic corticosteroid therapy, although recurrences follow discontinuation of therapy. Alopecia areata is occasionally associated with Hashimoto's thyroiditis, pernicious anemia, Addison's disease, and vitiligo.

Intralesional corticosteroids are frequently effective for alopecia areata. Triamcinolone acetonide in a con


centration of 2.5–10 mg/mL is injected in aliquots of 0.1 mL at approximately 1to 2-cm intervals, not exceeding a total dose of 30 mg per month for adults. Alternatively, anthralin 0.5% ointment, used daily, may help some patients. Alopecia areata is usually selflimiting, with complete regrowth of hair in 80% of patients, but some mild cases are resistant, as are the extensive totalis and universalis types. Both topical diphencyprone and squaric acid dibutylester, have been used to treat persistent alopecia areata. The principle is to sensitize the skin, then intermittently apply weaker concentrations to produce and maintain a slight dermatitis. Hair regrowth in 3–6 months in some patients has been reported to be remarkable. Long-term safety and efficacy have not been established. Support groups for patients with extensive alopecia areata are very beneficial. In trichotillomania (the pulling out of one's own hair), the patches of hair loss are irregular and growing hairs are always present, since they cannot be pulled out until they are long enough. The patches are often unilateral, occurring on the same side as the patient's dominant hand. The patient may be unaware of the habit.

Drug-induced alopecia is becoming increasingly important. Incriminated drugs include excessive and prolonged use of vitamin A, retinoids, antimitotic agents, anticoagulants, antithyroid drugs, oral contraceptives, trimethadione, allopurinol, propranolol, indomethacin, amphetamines, salicylates, gentamicin, and levodopa. While chemotherapy-induced alopecia is very distressing, it must be emphasized to the patient before treatment that it is invariably reversible.

Chartier MB et al: Approach to the adult female patient with diffuse nonscarring alopecia. J Am Acad Dermatol 2002;47: 809.

Ellis JA et al: Androgenetic alopecia: pathogenesis and potential for therapy. Expert Rev Mol Med 2002;2002:1.

Tosti A et al: Clobetasol propionate 0.05% under occlusion in the treatment of alopecia totalis/universalis. J Am Acad Dermatol 2003;49:96.


1. Morphologic Abnormalities of the Nails


Acquired nail disorders may be classified as local or those associated with systemic or generalized skin diseases.


  • Onycholysis (distal separation of the nail plate from the nail bed, usually of the fingers) is caused by excessive exposure to water, soaps, detergents, alkalies, and industrial cleaning agents. Candidal infection of the nail folds and subungual area, nail hardeners, and drug-induced photosensitivity may cause onycholysis, as may hyperthyroidism and hypothyroidism and psoriasis.

  • Distortion of the nail occurs as a result of chronic inflammation of the nail matrix underlying the eponychial fold. Such changes may also be caused by warts, tumors, or cysts, impinging on the nail matrix.

  • Discoloration and crumbly thickened nails are noted in dermatophyte infection and psoriasis.

  • Allergic reactions (to resins in undercoats and polishes or to nail glues) are characterized by onycholysis or by grossly distorted, hypertrophic, and misshapen nails.


  • Beau's lines (transverse furrows) may follow any serious systemic illness.

  • Atrophy of the nails may be related to trauma or to vascular or neurologic disease.

  • Clubbed fingers may be due to the prolonged hypoxemia associated with cardiopulmonary disorders. (See Chapter 9.)

  • Spoon nails may be seen in anemic patients.

  • Stippling or pitting of the nails is seen in psoriasis, alopecia areata, and hand eczema.

  • Nail hyperpigmentation may be caused by zidovudine, doxorubicin, cyclophosphamide, bleomycin, daunorubicin, fluorouracil, hydroxyurea, melphalan, mechlorethamine, and nitrosoureas.

Differential Diagnosis

Onychomycosis may cause nail changes identical to those seen in psoriasis. Careful examination for more characteristic lesions elsewhere on the body is essential to the diagnosis of the nail disorders. Cancer should be suspected (eg, Bowen's disease or squamous cell carcinoma) as the cause of any persistent solitary subungual or periungual lesion.


Toenail changes may lead to an ingrown nail—in turn often complicated by bacterial infection and occasionally by exuberant granulation tissue. Poor manicuring and poorly fitting shoes may contribute to this complication. Cellulitis may result.

Treatment & Prognosis

Treatment consists usually of careful debridement and manicuring and, above all, reduction of exposure to irritants (soaps, detergents, alkali, bleaches, solvents, etc). Longitudinal grooving due to temporary lesions of the matrix, such as warts, synovial cysts, and other impingements, may be cured by removal of the offending lesion.

If it is necessary to remove dystrophic nails for any reason (eg, fungal nails or severe psoriasis), a nonsurgical


method is to apply urea 40%, anhydrous lanolin 20%, white wax 5%, white petrolatum 25%, and silica gel type H. The nail folds are painted with compound tincture of benzoin and covered with cloth adhesive tape. The urea ointment is applied generously to the nail surface and covered with plastic film, and then adhesive tape. The ointment is left on for 5–10 days; then the nail plate may be curetted off. Medication can then be applied that is appropriate for the condition being treated.

2. Tinea Unguium (Onychomycosis)

Tinea unguium is a trichophyton infection of one or more (but rarely all) fingernails or toenails. The species most commonly found is T rubrum. “Saprophytic” fungi may rarely (< 5%) cause onychomycosis.

The nails are lusterless, brittle, and hypertrophic, and the substance of the nail is friable. Laboratory diagnosis is mandatory since only 50% of dystrophic nails are due to dermatophytosis. Portions of the nail should be cleared with 10% KOH and examined under the microscope for hyphae. Fungi may also be cultured. Periodic acid-Schiff stain of a histologic section of the nail plate will also demonstrate the fungus readily.

Onychomycosis is difficult to treat because of the long duration of therapy required and the frequency of recurrences. Fingernails respond more readily than toenails. For toenails, treatment is limited to patients with discomfort, inability to exercise, and immune compromise.

In general, systemic therapy is required to effectively treat nail onychomycosis. Topical therapy has limited value and the adjunctive value of surgical procedures is unproven. Fingernails can virtually always be cured and toenails are cured 35–50% of the time and are clinically improved about 75% of the time. In all cases, before treatment, the diagnosis should be confirmed. The costs of the various treatment options should be known and the most cost-effective treatment chosen. Drug interactions must be avoided. Ketoconazole, due to its higher risk for hepatotoxicity, is not recommended to treat any form of onychomycosis. For fingernails, ultramicronized griseofulvin 250 mg orally three times daily for 6 months can be effective. Alternative treatments are (in order of preference) oral terbinafine 250 mg/d for 6 weeks, oral itraconazole 400 mg/d for 7 days each month for 2 months, and oral itraconazole 200 mg/d for 2 months. Once clear, fingernails usually remain free of disease.

Onychomycosis of the toenails does not respond to griseofulvin therapy or topical treatments. The best treatment, which is also FDA approved, is oral terbinafine 250 mg daily for 12 weeks. Liver function tests and a complete blood count with platelets are performed monthly during treatment. A recently published alternative treatment schedule (but not confirmed by other workers) is oral terbinafine 250 mg/d for 1 week every 2 or 3 months for 1 year (four or six treatment pulses). Pulse oral itraconazole 200 mg twice daily for 1 week per month for 3 months is inferior to standard terbinafine treatments, but it is an acceptable alternative for those unable to take terbinafine.

For recurrent disease, terbinafine can be given as pulse therapy, 250 mg/d orally for 1 week every month for 12 months, or the standard 3 months of oral daily treatment of 250 mg/d can be given and repeated again 6 months following the first course (treat months 1 to 3 and 9 to 12).

Casciano J et al: Economic analysis of oral and topical therapies for onychomycosis of the toenails and fingernails. Manag Care 2003;12:47.

Heikkila H et al: Long-term results in patients with onychomycosis treated with terbinafine or itraconazole. Br J Dermatol 2002;146:250.

Mayeaux EJ Jr: Nail disorders. Prim Care 2000;27:333.

Pavlotsky F et al: Pulsed versus continuous terbinafine dosing in the treatment of dermatophyte onychomycosis. J Dermatolog Treat 2004;15:315.

Wilcock M et al: Inappropriate use of oral terbinafine in family practice. Pharm World Sci 2003;25:25.

Zaias N et al: The successful treatment of Trichophyton rubrum nail bed (distal subungual) onychomycosis with intermittent pulse-dosed terbinafine. Arch Dermatol 2004;140:691.



  • Usually, abrupt onset of widespread, symmetric erythematous eruption.

  • May mimic any inflammatory skin condition.

  • Constitutional symptoms (malaise, arthralgia, headache, and fever) may be present.

General Considerations

As is well recognized, only a minority of cutaneous drug reactions result from allergy. True allergic drug reactions involve prior exposure, an “incubation” period, reactions to doses far below the therapeutic range, manifestations different from the usual pharmacologic effects of the drug, involvement of only a small portion of the population at risk, restriction to a limited number of syndromes (anaphylactic and anaphylactoid, urticarial, vasculitic, etc), and reproducibility.

Rashes are among the most common adverse reactions to drugs and occur in 2–3% of hospitalized patients. Amoxicillin, trimethoprim-sulfamethoxazole, and ampicillin or penicillin are the most common causes of urticarial and maculopapular reactions. Toxic epidermal necrolysis and Stevens-Johnson syndrome are most commonly produced by sulfonamides and anticonvulsants. Phenolphthalein, pyrazolone derivatives, tetracyclines, NSAIDs, trimethoprim-sulfamethoxazole, and barbiturates are the major causes of fixed drug eruptions.

Table 6-4. Skin reactions due to systemic drugs.

Reaction Appearance Distribution and Comments Common Offenders
Toxic erythema Morbilliform, maculopapular, exanthematous reactions. The most common skin reaction to drugs. Often more pronounced on the trunk than on the extremities. In previously exposed patients, the rash may start in 2–3 days. In the first course of treatment, the eruption often appears about the seventh to ninth days.
Fever may be present.
Antibiotics (especially ampicillin and trimethoprim-sulfamethoxazole), sulfonamides and related compounds (including thiazide diuretics, furosemide, and sulfonylurea hypoglycemic agents), and barbiturates.
Erythema multiforme major Target-like lesions.
Bullae may occur.
Mucosal involvement.
Mainly on the extensor aspects of the limbs. Sulfonamides, penicillamine, barbiturates, and NSAIDs.
Erythema nodosum Inflammatory cutaneous nodules. Usually limited to the extensor aspects of the legs. May be accompanied by fever, arthralgias, and pain. Oral contraceptives.
Allergic vasculitis Inflammatory changes may present as urticaria that lasts over 24 hours, hemorrhagic papules (“palpable purpura”), vesicles, bullae, or necrotic ulcers. Most severe on the legs. Sulfonamides, indomethacin, phenytoin, allopurinol, and ibuprofen.
Purpura Itchy, petechial macular rash. Dependent areas. Results most typically from thrombocytopenia. Thiazides, sulfonamides, sulfonylureas, barbiturates, quinine, and sulindac.
Eczema Similar to contact dermatitis. A rare reaction in patients previously sensitized by external exposure who are given the same or a related substance systemically. Penicillin, neomycin, phenothiazines, and local anesthetics.
Exfoliative dermatitis and erythroderma Red and scaly. Entire skin surface. Allopurinol, sulfonamides, isoniazid, gold, or carbamazepine.
Photosensitivity: increased sensitivity to light, often of ultraviolet A wavelengths, but may be due to UVB or visible light as well Sunburn, vesicles, papules in photodistributed pattern. Exposed skin of the face, the neck, and the backs of the hands and, in women, the lower legs. Exaggerated response to ultraviolet light. Sulfonamides and sulfonamide-related compounds (thiazide diuretics, furosemide, sulfonylureas), tetracyclines, phenothiazines, sulindac, amiodarone, and NSAIDs.
Drug-related lupus erythematosus May present with a photosensitive rash accompanied by fever, polyarthritis, myalgia, and serositis. Less severe than systemic lupus erythematosus, sparing the kidneys and central nervous system. Recovery often follows drug withdrawal. Hydralazine, procainamide; less often, isoniazid, phenytoin, lisinopril, hydro-chlorothiazide; diltiazem; may cause subacute lupus erythematosus.
Lichenoid and lichen planus–like eruptions Pruritic, erythematous to violaceous polygonal papules that coalesce or expand to form plaques. May be in photoor nonphotodistributed pattern. Bismuth, carbamazepine, chlordiazepoxide, chloroquine, chlorpropamide, dapsone, ethambutol, furosemide, gold salts, hydroxychloroquine, methyldopa, penicillamine, phenothiazines, propranolol, quinidine, quinine, quinacrine, streptomycin, sulfonylureas, tetracyclines, thiazides, and triprolidine.
Fixed drug eruptions Single or multiple demarcated, round, erythematous plaques that often become hyperpigmented. Recur at the same site when the drug is repeated. Hyperpigmentation, if present, remains after healing. Numerous drugs, including antimicrobials, analgesics, barbiturates, cardiovascular drugs, heavy metals, antiparasitic agents, antihistamines, phenolphthalein, ibuprofen, and naproxen.
Toxic epidermal necrolysis Large sheets of erythema, followed by separation, which looks like scalded skin. Rare. In adults, the eruption has occurred after administration of many classes of drugs, particularly anticonvulsants, antibiotics, sulfonamides, and NSAIDs.
Urticaria Red, itchy wheals that vary in size from < 1 cm to many centimeters. May be accompanied by angioedema. Chronic urticaria is rarely caused by drugs. Acute urticaria: penicillins, NSAIDs, sulfonamides, opiates, and salicylates.
Angioedema is common in patients receiving ACE inhibitors.
Pruritus Itchy skin without rash.   Pruritus ani may be due to overgrowth of candida after systemic antibiotic treatment. NSAIDs may cause pruritus without a rash.
Hair loss   Hair loss most often involves the scalp, but other sites may be affected. A predictable side effect of cytotoxic agents and oral contraceptives. Diffuse hair loss also occurs unpredictably with a wide variety of other drugs, including anticoagulants, antithyroid drugs, newer antimicrobials, cholesterol-lowering agents, heavy metals, corticosteroids, androgens, NSAIDs, retinoids (isotretinoin, etretinate), and β-blockers.
Pigmentary changes Flat hyperpigmented areas Forehead and cheeks (chloasma, melasma). The most common pigmentary disorder associated with drug ingestion. Improvement is slow despite stopping the drug. Oral contraceptives are the usual cause.
Blue-gray discoloration. Light-exposed areas. Chlorpromazine and related phenothiazines.
Brown or blue-gray pigmentation. Generalized. Heavy metals (silver, gold, bismuth, and arsenic). Arsenic, silver, and bismuth are not used therapeutically, but patients who receive gold for rheumatoid arthritis may show this reaction.
Yellow color. Generalized. Usually quinacrine.
Blue-black patches on the shins.   Minocycline, chloroquine.
Blue-black pigmentation of the nails and palate and depigmentation of the hair.   Chloroquine.
Slate-gray color. Primarily in photoexposed areas. Amiodarone.
Brown discoloration of the nails. Especially in more darkly pigmented patients. Zidovudine (azidothymidine; AZT), hydroxyurea.
Psoriasiform eruptions Scaly red plaques. May be located on trunk and extremities. Palms and soles may be hyperkeratotic. May cause psoriasiform eruption or worsen psoriasis. Chloroquine, lithium, β-blockers, and quinacrine.
Pityriasis rosea–like eruptions Oval, red, slightly raised patches with central scale. Mainly on the trunk. Barbiturates, bismuth, captopril, clonidine, gold salts, methopromazine, metoprolol, metronidazole, and tripelennamine.
NSAIDs = nonsteroidal anti-inflammatory drugs; ACE = angiotensin-converting enzyme.




Clinical Findings


The onset is usually abrupt, with bright erythema and often severe itching, but may be delayed. Fever and other constitutional symptoms may be present. The skin reaction usually occurs in symmetric distribution.

Table 6-4 summarizes the types of skin reactions, their appearance and distribution, and the common offenders in each case.


Routinely ordered blood work is of no value in the diagnosis of drug eruptions. However, skin biopsies may be helpful in making the diagnosis.

Differential Diagnosis

Observation after discontinuation, which may be a slow process, helps establish the diagnosis. Rechallenge, though of theoretical value, may pose a danger to the patient and is best avoided.


Some cutaneous drug reactions may be associated with a clinical complex involving other organs (complex drug reactions). The organ systems involved depend on the individual medication or drug class. Most common is an infectious mononucleosis-like illness and hepatitis associated with administration of anticonvulsants.



Systemic manifestations are treated as they arise (eg, anemia, icterus, purpura). Antihistamines may be of value in urticarial and angioneurotic reactions. Epinephrine 1:1000, 0.5–1 mL intravenously or subcutaneously, should be used as an emergency measure. In severe cases, corticosteroids may be used at doses similar to those used for acute contact dermatitis.


Extensive blistering eruptions resulting in erosions and superficial ulcerations demand hospitalization and nursing care as for burn patients.


Drug rash usually disappears upon withdrawal of the drug and proper treatment.

Baba M et al: The anticonvulsant hypersensitivity syndrome. J Eur Acad Dermatol Venereol 2003;17:399.

Devos SA et al: Adverse skin reactions to anti-TNF-alpha monoclonal antibody therapy. Dermatology 2003;206:388.

Dunn N: 10-minute consultation: adverse drug event. BMJ 2003;326:1018.

Lerch M et al: The immunological and clinical spectrum of delayed drug-induced exanthems. Curr Opin Allergy Clin Immunol 2004;4:411.

Wolf R et al: Treatment of toxic epidermal necrolysis syndrome with “disease modifying” drugs: the controversy goes on. Clin Dermatol 2004;22:267.


*Hirsutism is discussed in Chapter 26.

Current Medical Diagnosis & Treatment 2006
Current Medical Diagnosis & Treatment, 2006 (Current Medical Diagnosis and Treatment)
ISBN: 0071454101
EAN: 2147483647
Year: 2006
Pages: 71

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