CASE REPORT article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
This article is part of the Research TopicThe Association of Other Autoimmune Diseases in Patients with Thyroid Autoimmunity: Volume IIView all 27 articles
Case Report: Anti–TNF-α Therapy–Associated Destructive Thyroiditis and Unmasking of Latent Amyloid A Amyloidosis in Rheumatoid Arthritis
Provisionally accepted
- 1Department of Orthopaedic Surgery, Shiga University of Medical Science, Otsu, Japan
- 2Department of Orthopaedics, Kyoto Okamoto Memorial Hospital, Kyoto, Japan
- 3Department of Spine and Joint Reconstruction, Shiga University of Medical Science, Otsu, Japan
- 4Department of Sports and Muscloskeletal Medicine, Shiga University of Medical Science, Otsu, Japan
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Introduction: Tumor necrosis factor (TNF)-α inhibitors are widely used for rheumatoid arthritis (RA), but paradoxical immune reactions, including autoimmune thyroid disease, have been reported. Case presentation: 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. Conclusion: 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.
Keywords: AA amyloidosis, Anti-TNF therapy, Destructive thyroiditis, Multiple Organ Failure, Rheumatoid arthritis
Received: 16 Dec 2025; Accepted: 09 Feb 2026.
Copyright: © 2026 Kumagai, Okumura, Mimura, Yayama, Kubo and Imai. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Kosuke Kumagai
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