S4925 Recurrent TNF-Inhibitor-Induced Thyroiditis in a Patient With Crohn’s Disease

Introduction: TNF-inhibitors (TNFi) are widely-used for immune-mediated diseases such as Crohn’s disease. Thyroiditis is a rare complication of TNFi use in patients with Crohn’s disease without primary thyroid disease. Case Description/Methods: A Crohn’s patient on 6 months of adalimumab, with no known history of thyroid disease, presented to the emergency room with new-onset palpitations. Work up revealed supraventricular tachycardia, a suppressed thyroid-stimulating hormone (<0.01 uIU/mL, nl: 0.4–4.2), and high free t4 (2.64 ng/dL, nl: 0.82–1.77). Thyroid antibodies (thyroid-stimulating immunoglobulin, thyrotropin receptor antibody, and anti-thyroid peroxidase antibodies) were negative and a thyroid ultrasound was normal. Adalimumab was held and methimazole was started for a total of 18 months due to concern for drug-induced thyroiditis. Thyroid function tests (TFTs) normalized in 4 months with resolution of palpitations. Four years later, due to poorly controlled Crohn’s disease on upadacitinib, he was started on infliximab. His abdominal pain and diarrhea improved, however after 3 months of therapy he developed palpitations, anxiety and insomnia. TFTs again showed a suppressed thyroid-stimulating hormone (<0.01 uIU/mL, nl: 0.4–4.2) and high free t4 (2.11 ng/dL, nl: 0.80–1.5). Thyroid antibodies were again negative. He was advised to stop infliximab and methimazole was re-started. His TFTs normalized within 2 weeks, and all other symptoms of hyperthyroidism resolved. Discussion: TNFi can have unpredictable effects on thyroid function. We report a case of recurrent thyroiditis resulting in symptomatic hyperthyroidism in a patient treated with 2 different TNFi, suggesting a class effect. In both instances, TNFi cessation and use of methimazole resolved the hyperthyroidism. Although no evidence of autoimmune thyroid disease was found, it has been reported that antibodies against TNFi may cause thyroid gland damage, usually after 3 to 6 months of treatment, suggesting a drug-antibody mechanism. Absence of viral prodrome and recurrence after re-exposure made viral thyroiditis unlikely. Thyroid disease while on TNFi drugs should not delay treatment with these agents, but rather result in clinicians having a low threshold for suspecting drug-induced thyroiditis if there is an acute worsening.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001147160.94838.bc
Primary Topic
Rheumatoid Arthritis Research and Therapies
Type
article
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article

S4925 Recurrent TNF-Inhibitor-Induced Thyroiditis in a Patient With Crohn’s Disease

Richard Vaca, Ayanna Lewis
The American Journal of Gastroenterology
Rheumatoid Arthritis Research and Therapies
article

S4925 Recurrent TNF-Inhibitor-Induced Thyroiditis in a Patient With Crohn’s Disease

Richard Vaca, Ayanna Lewis
article en

Abstract

Introduction: TNF-inhibitors (TNFi) are widely-used for immune-mediated diseases such as Crohn’s disease. Thyroiditis is a rare complication of TNFi use in patients with Crohn’s disease without primary thyroid disease. Case Description/Methods: A Crohn’s patient on 6 months of adalimumab, with no known history of thyroid disease, presented to the emergency room with new-onset palpitations. Work up revealed supraventricular tachycardia, a suppressed thyroid-stimulating hormone (<0.01 uIU/mL, nl: 0.4–4.2), and high free t4 (2.64 ng/dL, nl: 0.82–1.77). Thyroid antibodies (thyroid-stimulating immunoglobulin, thyrotropin receptor antibody, and anti-thyroid peroxidase antibodies) were negative and a thyroid ultrasound was normal. Adalimumab was held and methimazole was started for a total of 18 months due to concern for drug-induced thyroiditis. Thyroid function tests (TFTs) normalized in 4 months with resolution of palpitations. Four years later, due to poorly controlled Crohn’s disease on upadacitinib, he was started on infliximab. His abdominal pain and diarrhea improved, however after 3 months of therapy he developed palpitations, anxiety and insomnia. TFTs again showed a suppressed thyroid-stimulating hormone (<0.01 uIU/mL, nl: 0.4–4.2) and high free t4 (2.11 ng/dL, nl: 0.80–1.5). Thyroid antibodies were again negative. He was advised to stop infliximab and methimazole was re-started. His TFTs normalized within 2 weeks, and all other symptoms of hyperthyroidism resolved. Discussion: TNFi can have unpredictable effects on thyroid function. We report a case of recurrent thyroiditis resulting in symptomatic hyperthyroidism in a patient treated with 2 different TNFi, suggesting a class effect. In both instances, TNFi cessation and use of methimazole resolved the hyperthyroidism. Although no evidence of autoimmune thyroid disease was found, it has been reported that antibodies against TNFi may cause thyroid gland damage, usually after 3 to 6 months of treatment, suggesting a drug-antibody mechanism. Absence of viral prodrome and recurrence after re-exposure made viral thyroiditis unlikely. Thyroid disease while on TNFi drugs should not delay treatment with these agents, but rather result in clinicians having a low threshold for suspecting drug-induced thyroiditis if there is an acute worsening.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 44%
Rheumatoid Arthritis Research and Therapies
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