Case Report: Anti–TNF-α therapy–associated destructive thyroiditis and unmasking of latent amyloid A amyloidosis in rheumatoid arthritis

TL;DR

A man with rheumatoid arthritis developed thyroiditis and revealed hidden amyloidosis after anti-TNF-α therapy, showing the need for monitoring during such treatments.

Contribution

This case report reveals a rare but important side effect of anti-TNF-α therapy in RA patients, linking it to unmasking latent amyloidosis and inducing autoimmune thyroiditis.

Findings

Anti-TNF-α therapy led to destructive thyroiditis in a patient with rheumatoid arthritis.

Latent amyloid A amyloidosis was revealed following immune modulation by the anti-TNF-α biologic.

Treatment with an IL-6 receptor antibody improved symptoms and normalized inflammatory markers.

Abstract

Tumor necrosis factor (TNF)-α inhibitors are widely used for rheumatoid arthritis (RA), but paradoxical immune reactions, including autoimmune thyroid disease, have been reported.

We describe a 71-year-old man with a 16-year history of RA who developed destructive thyroiditis after initiation of certolizumab pegol. Despite symptom resolution, he subsequently developed acute renal failure and diarrhea. Biochemical and histological analyses revealed elevated serum amyloid A (AA) and amyloid deposition in the kidney and duodenum, confirming AA amyloidosis. We considered that the latent amyloidosis became clinically apparent following immune modulation by the anti-TNF-α biologic. Treatment with the IL-6 receptor antibody tocilizumab rapidly normalized inflammatory markers and improved both renal function and gastrointestinal symptoms.

This case highlights that TNF-α inhibition may paradoxically unmask underlying amyloidosis and induce autoimmune thyroiditis. Clinicians should monitor thyroid and systemic amyloid markers when introducing biologic therapy for long-standing RA.

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