Increased risk of thyroid autoimmunity in rheumatoid arthritis.

Abstract

Two interesting papers on thyroid autoimmunity in patients with rheumatoid arthritis were recently published [1, 2]. Thyroid autoimmunity is the most common autoimmune disease, and frequently observed together with other autoimmune diseases, including rheumatoid arthritis. Both diseases are probably caused by a combination of innate and adaptive immune regulatory abnormalities, and both are diagnosed in the clinical setting by measurement of their relevant autoantibodies [thyroperoxidase (TPO) and thyrotropin receptor antibodies (TRAb), and non-organspecific autoantibodies, respectively]. Non-organ-specific antibodies have been demonstrated in up to 25 % of patients with autoimmune thyroid diseases in smaller series [3], and sometimes the phenotypically clinical diseases exist in the same patients. Several previous studies of smaller series also found thyroid autoantibodies in patients with rheumatoid arthritis, but not until now has a systematic review and meta-analysis been performed [1]. The authors performed a thorough literature search and included a total of 1021 patients with rheumatoid arthritis and 1500 healthy controls. The authors only included anti-TPO and thyroglobulin antibodies (TgAb), leaving out TRAb, which are pathognomonic for Graves’ disease, and extracted only 13 studies from a total of 439 articles with relevant data. The results of the meta-analysis showed that the prevalence of thyroid autoantibody positivity in patients with rheumatoid arthritis was higher than that in healthy controls (TgAb: OR 3.17, 95 % CI 2.24–4.49; TPOAb: OR 2.33, 95 % CI 1.24–4.39). The results of this meta-analysis suggested that thyroid autoimmunity is more prevalent in patients with rheumatoid arthritis than in the control population. However, the meta-analysis does not discuss the fact that anti-TPO and TgAb are present in the majority of patients with chronic autoimmune hypothyroidism, such as Hashimoto’s and atrophic thyroiditis, but that they are also present in a large proportion of patients with Graves’ disease, together with TRAb. It is therefore not possible to disclose from the publication which clinical disease was more prevalent in the original studies or the meta-analysis. The general clinical impression is that Graves’ disease rather than Hashimoto’s thyroiditis is often seen together with rheumatoid arthritis, although this has never been documented. It is thus unfortunately not possible to predict which elevated thyroid autoimmunity risk to expect from the meta-analysis, and therefore not feasible to provide recommendations for follow-up of possible thyroid autoimmunity in patients with rheumatoid arthritis. Future studies are needed for this purpose. A very good reason to perform such a study would be to predict induction or progression of thyroid autoimmunity using biological anti-rheumatic agents for treatment of rheumatoid arthritis, as done in the second study [2]. The authors of this publication studied prospectively 36 patients with rheumatoid arthritis treated for 3 years with Infliximab (N = 18) or Rituximab (N = 18), respectively. The patients were compared with three control groups: Twentyeight rheumatic patients treated with disease-modifying anti-rheumatic drugs and/or glucocorticoids, 21 rheumatic patients not receiving any treatment, and 49 healthy individuals. All patients had their thyroid function assessed together with thyroid autoantibodies and ultrasonography. Thyroid function was measured by serum TSH, free T4 & Ulla Feldt-Rasmussen ufeldt@rh.dk