Rheumatic Manifestations of Endocrine Diseases

Joseph A. Markenson


Curr Opin Rheumatol. 2010;22(1):64-71. 

In This Article

Thyroid Disorders in Patients with Connective Disease

The occurrence of chronic autoimmune thyroiditis (Hashimoto's thyroiditis) as well as hypothyroidism is common in the general population[12] making it difficult to ascertain whether the incidence of either is increased in patients with connective tissue disease. Two exceptions may be scleroderma in which fibrosis is the cause of hypothyroidism and congenital heart block in children of hypothyroid anti-Ro+ mothers. Medications used to treat various connective diseases as well as the disease itself can affect thyroid function. For example, glucocorticoids inhibit TSH secretion slightly lowering serum thyroid hormone concentrations. Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDS) may lower serum thyroid hormone by interfering with binding to their carrier proteins.

In other illnesses such as systemic lupus erythematosus (SLE) 15–20% of patients have antithyroid antibodies.[13] Concomitant hypothyroidism is estimated at 5.7% (five times greater than expected) as opposed to hyperthyroidism occurring at 1.7% (similar to the normal population). This association may be genetic as noted in a study of multiplex SLE families in which 35 who also had autoimmune thyroid disease demonstrated a linkage with 5q14.3–15 (major susceptibility locus for SLE also found in auto immune thyroid disease). This suggests that 5q14.3–15 harbors a susceptibility gene shared by patients with SLE and autoimmune thyroid disease.[14]

A common reason for referral to a rheumatologist is often a young female patient with arthralgia whom the referring physician has obtain a blood sample testing positive for antinuclear antibody (ANA). Studies of patients with Graves' disease and chronic autoimmune thyroiditis have demonstrated upwards of 26% positivity for ANA and 34% anti-single-stranded DNA antibodies. No patients in these studies had antibodies to double-stranded DNA, or extractable nuclear antigens (anti-Ro/SSA, anti-La/SSB, anti-SM or anti-RNP).[15]

With respect to polymyalgia rheumatic and giant cell arthritis few studies are available with some demonstrating a relationship[16] but most reporting no association.[17,18] However, the occurrence of polymyalgia rheumatic or giant cell arthritis may be more common in patients with autoimmune thyroid disease.[19]

In fibromyalgia an attenuated response of TSH to thryotropin-releasing hormone (TRH) as well an increased prevalence of antithyroid antibodies compared with controls has been reported (clinical significance unknown).[20,21]


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.