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Chapter 48 Endocrine Arthropathies

Manual of Rheumatology and Outpatient Orthopedic Disorders

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Chapter 48 Endocrine Arthropathies

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Michael D. Lockshin

Pathogenesis and clinical manifestations
Diagnosis
Laboratory studies
Differential diagnosis
Treatment and prognosis

I. Pathogenesis and clinical manifestations. The musculoskeletal manifestations of endocrine diseases are highly variable. They include muscle dysfunction, disorders of bone metabolism, and cartilage deformation. Tendons, ligaments, and tendon attachment sites are regularly symptomatic. Crystal arthropathies and calcific tendinitis may be symptoms of endocrine disease. Table 48-1 lists the rheumatic manifestations of common endocrinopathies.

Table 48-1. Rheumatic manifestations and pathogenesis of common endocrinopathies

II. Diagnosis. Endocrinopathic musculoskeletal disease tends to be diffuse and poorly described. Except for crystal arthritis, it is more often periarticular than articular. The most important diagnostic step is to consider the possibility of endocrinopathy, then to evaluate whether the patient's symptoms might be explained by that abnormality. History, physical examination, and often radiology define the rheumatologic problem, and directed laboratory studies define the associated endocrinopathy.

1. Myalgias, proximal myopathies, and, on occasion, high levels of creatine kinase suggest thyroid disorders. Less commonly, acromegaly and disorders causing hyperkalemia or hypokalemia will suggest primary muscle weakness. Carpal tunnel syndrome occurs in hypothyroidism , acromegaly, and diabetes. Scleredema of the upper back is characteristic of diabetes.
2. Parathyroid disorders, acromegaly, most heritable disorders (Marfan syndrome, pseudo-hypoparathyroidism, ochronosis), and advanced diabetes show typical radiologic abnormalities.
3. Osteopenia is characteristic of hyperparathyroidism and hyperadrenalism, but it also occurs in patients with thyroid and pituitary dysfunction.
4. Characteristic syndromes may be diagnostic; the cheiropathy of advanced diabetes and thyroid acropathy in Graves' disease are examples. Chondrocalcinosis and characteristic metacarpophalangeal disease are diagnostic of hemochromatosis.

III. Laboratory studies. Radiographs often first suggest the possibility of an endocrinopathy. Routine clinical laboratory tests are usually not helpful. It is necessary to confirm the suspected endocrinopathy with appropriately directed tests.

IV. Differential diagnosis. Rheumatoid arthritis and osteoarthritis , gout, pseudogout, lupus, dermatomyositis, and scleroderma may each be suggested by some manifestation of an endocrinopathy. Normal levels of antinuclear antibody, rheumatoid factor, and muscle enzymes, and a normal erythrocyte sedimentation rate exclude these diagnoses, but abnormal test results do not positively confirm them. A noninflammatory synovial fluid analysis (except in pseudogout associated with diabetes, hyperparathyroidism, or hemochromatosis) is most characteristic of endocrinopathy. In myxedema, synovial fluid is often very viscous and colorless.

V. Treatment and prognosis

1. Treatment of the underlying endocrinopathy relieves myalgia, myopathy, tendinitis, and, to some extent, osteopenia and skin manifestations, but it will not reverse established bone and cartilage deformity. The rate of remission varies with the endocrinopathy.
   1. In thyroid disease, myalgias remit within weeks to months, myopathy within months, and acropachy in years , if at all.
   2. In parathyroid disease, bone pain abates in months, and bone remineralization occurs within years. Normal bone structure may not be completely restored, particularly if bone trabeculae have become discontinuous.
   3. Adrenal myopathy improves in months.
   4. The skeletal changes of pituitary, gonadal, and congenital endocrinopathies usually do not regress. Estrogen replacement retards bone loss, but remineralization of osteoporotic bone requires calcium, calcitonin, and bisphosphonate therapy .
   5. The skeletal and soft- tissue abnormalities of diabetes and hemochromatosis do not improve.
2. Medical treatment (other than treatment of the endocrinopathy) is nonspecific and symptomatic. Nonsteroidal antiinflammatory drugs and analgesics are commonly used. There is no role for corticosteroid preparations , antimalarial agents , disease-modifying antirheumatic drugs (DMARDs), or immunosuppressive drugs. The following specific precautions are necessary:
   1. Patients with hyperthyroidism metabolize drugs rapidly ; standard doses may be ineffective .
   2. Patients with hypothyroidism metabolize drugs slowly; standard doses may be toxic.
   3. In diabetes and hyperparathyroidism, renal dysfunction should be anticipated.
   4. In hemochromatosis, hepatic dysfunction should be anticipated.
3. Surgical treatment is useful for carpal tunnel syndrome and, on occasion, for orthopedic repair, but specific concerns are as follows :
   1. Osteopenic bones heal and hold prostheses poorly.
   2. Charcot's joints heal poorly and refracture. Fusions may be indicated.
   3. Diabetic cheiropathy responds very poorly to attempts at surgical correction.

Bibliography

Askari AD, et al. Arthritis of hemochromatosis. Am J Med 1983;75:957.

Benedetti A, et al. Joint lesions in diabetes. N Engl J Med 1975;282:1033.

Clouse ME, et al. Diabetic osteoarthropathy: clinical and roentgenographic observations in 90 cases. Am J Roentgenol Radiat Ther 1974;121:22.

Fatomechi V, et al. Dermopathy of Graves' disease (pretibial myxedema). Review of 150 cases. Medicine (Baltimore) 1994;73:1.

Grigic A, et al. Joint contracture in childhood diabetes. N Engl J Med 1975;292:371.

Lieberman S, et al. Rheumatologic and skeletal changes in acromegaly. Endocrinol Metab Clin North Am 1992;21:615.

McLean RM, et al. Bone and joint manifestations of hypothyroidism. Semin Arthritis Rheum 1995;24:282.

Poa HL, et al. Thyroid-induced osteoporosis. Curr Opin Orthop 1995;6:39.

Rosenbloom AL, et al. Limited joint mobility in childhood diabetes mellitus indicates increased risk for microvascular disease. N Engl J Med 1983;305:191.

Ross DS. Hyperthyroidism, thyroid hormone and bone. Thyroid 1994;4:319.

Books@Ovid
Copyright 2000 by Lippincott Williams & Wilkins
Stephen A. Paget, M.D., Allan Gibofsky, M.D., J.D. and John F. Beary, III, M.D.
Manual of Rheumatology and Outpatient Orthopedic Disorders

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