Abstract
Objective Rheumatoid arthritis (RA) is characterized by high levels of cytokines such as tumor necrosis factor (TNF). TNF appears to have an etiologic role in thyroid dysfunction, and thyroid dysfunction is a common comorbidity in RA. Anti-TNF treatment might limit thyroid dysfunction. Thus, changes in thyroid hormones were studied during TNF-blocking therapy in patients with RA.
Methods At baseline and after 6 months’ treatment with adalimumab, thyroid function [thyroid-stimulating hormone (TSH), free thyroxine (fT4), and antibodies against thyroid peroxidase (TPOabs)] were assessed in 138 consecutive adalimumab-treated patients with RA who were naive for TNF-blocking agents. Patients were categorized as hypothyroid, hyperthyroid, or euthyroid. In these groups, changes in thyroid function were determined.
Results Prevalences of hypothyroidism, hyperthyroidism, and TPOabs were 13%, 5%, and 15%, respectively. After 6 months, TPOabs decreased from 267 to 201 IU/ml (p = 0.048). In hypothyroid patients without concomitant L-thyroxine, a trend for declining levels of TSH was observed. Subgroup analysis revealed that in patients who were hypothyroid and TPOabs-positive and L-thyroxine-naive, TSH levels decreased significantly, from 12.5 (interquartile range 6.7–18.4) to 7.1 (interquartile range 4.9–13.8) mU/l (p = 0.043).
Conclusion Anti-TNF treatment improves thyroid function in hypothyroid patients with RA (especially in those who are L-thyroxine-naive and TPOabs-positive), providing further evidence that inflammatory cytokines such as TNF have a pathogenic role in thyroid dysfunction.
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