Thyroid hormone changes after tumor necrosis factor inhibitor therapy in euthyroid patients with rheumatic diseases

Abstract

Background/aim: Tumor necrosis factor-alpha (TNF-α) plays a central role in chronic inflammatory diseases. Anti-TNF agents are widely used in rheumatological conditions; however, their association with thyroid hormone parameters in patients without pre-existing thyroid disease remains incompletely understood. This study aimed to evaluate changes in thyroid hormone profiles during anti-TNF therapy in euthyroid patients with rheumatic diseases. Methods: In this retrospective study, 98 patients diagnosed with rheumatoid arthritis, ankylosing spondylitis, or Behçet’s disease without known thyroid disease were evaluated. Thyroid function tests, including thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxine (fT4), anti-thyroid peroxidase (anti-TPO) antibodies, inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), and metabolic parameters were assessed at baseline and after 3 and 6 months of anti-TNF therapy. Results: Anti-TNF therapy was associated with significant reductions in inflammatory markers (CRP and ESR, p < 0.01). A modest decrease in fasting glucose levels and an increase in high-density lipoprotein cholesterol (HDL-C) were observed during follow-up (p = 0.024 and p = 0.044, respectively). TSH and fT4 levels remained stable over time, whereas a gradual increase in fT3 levels was observed (p < 0.01). No significant changes were detected in anti-TPO antibody levels. Conclusions: Among euthyroid patients with rheumatic diseases, predominantly rheumatoid arthritis and ankylosing spondylitis, anti-TNF therapy was associated with stable thyroid function parameters. The observed increase in fT3 levels may reflect reduced inflammatory burden rather than direct thyroidal effects. These findings support the thyroid safety of anti-TNF agents while highlighting potential links between inflammation control and peripheral thyroid hormone conversion.