{"title":"Subacute thyroiditis during anti-programmed cell death protein 1 antibody therapy: A case report","authors":"Makiko Ikemoto , Yasufumi Seki , Daisuke Watanabe , Toshio Takagi , Atsuhiro Ichihara","doi":"10.1016/j.thscie.2025.100024","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><div>Immune checkpoint inhibitor (ICI) therapies can occasionally induce thyrotoxicosis as an ICI-associated adverse effect. The etiology of thyrotoxicosis during ICI therapy is painless thyroiditis, which is classified as destructive thyroiditis, in most cases. However, another form of destructive thyroiditis, subacute thyroiditis, has rarely been reported. Here, we present a case of subacute thyroiditis that emerged during anti-programmed cell death protein 1 (PD-1) antibody pembrolizumab therapy.</div></div><div><h3>Case presentation</h3><div>A 45-year-old man underwent pembrolizumab therapy after undergoing heminephrectomy for renal cell carcinoma. Two weeks after the 6th dose of pembrolizumab, administered 27 weeks following the initial administration, the patient complained of neck pain alongside increased levels of serum C-reactive protein and thyroid hormones, despite the absence of infectious symptoms. Upon thyroid echography, a hypoechoic lesion was observed, and technetium-99m thyroid scintigraphy revealed reduced thyroid uptake, the patient was diagnosed with subacute thyroiditis. Treatment with a maximum dose of 20 mg of prednisolone for 4 weeks normalized thyroid hormone levels, which remained within the normal range throughout the subsequent three courses of pembrolizumab therapy.</div></div><div><h3>Conclusion</h3><div>We present a case of subacute thyroiditis during pembrolizumab therapy, highlighting the importance of investigating the etiology of thyrotoxicosis during ICI therapy and proposing a potential association between ICI therapy and the development of subacute thyroiditis.</div></div>","PeriodicalId":101253,"journal":{"name":"Thyroid Science","volume":"2 2","pages":"Article 100024"},"PeriodicalIF":0.0000,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Thyroid Science","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2950300025000023","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Introduction
Immune checkpoint inhibitor (ICI) therapies can occasionally induce thyrotoxicosis as an ICI-associated adverse effect. The etiology of thyrotoxicosis during ICI therapy is painless thyroiditis, which is classified as destructive thyroiditis, in most cases. However, another form of destructive thyroiditis, subacute thyroiditis, has rarely been reported. Here, we present a case of subacute thyroiditis that emerged during anti-programmed cell death protein 1 (PD-1) antibody pembrolizumab therapy.
Case presentation
A 45-year-old man underwent pembrolizumab therapy after undergoing heminephrectomy for renal cell carcinoma. Two weeks after the 6th dose of pembrolizumab, administered 27 weeks following the initial administration, the patient complained of neck pain alongside increased levels of serum C-reactive protein and thyroid hormones, despite the absence of infectious symptoms. Upon thyroid echography, a hypoechoic lesion was observed, and technetium-99m thyroid scintigraphy revealed reduced thyroid uptake, the patient was diagnosed with subacute thyroiditis. Treatment with a maximum dose of 20 mg of prednisolone for 4 weeks normalized thyroid hormone levels, which remained within the normal range throughout the subsequent three courses of pembrolizumab therapy.
Conclusion
We present a case of subacute thyroiditis during pembrolizumab therapy, highlighting the importance of investigating the etiology of thyrotoxicosis during ICI therapy and proposing a potential association between ICI therapy and the development of subacute thyroiditis.