Immune checkpoint inhibitor-related thyroid dysfunction.
PD-1
PD-L1
hyperthyroidism
hypothyroidism
irAE
thyrotoxicosis
Journal
Best practice & research. Clinical endocrinology & metabolism
ISSN: 1878-1594
Titre abrégé: Best Pract Res Clin Endocrinol Metab
Pays: Netherlands
ID NLM: 101120682
Informations de publication
Date de publication:
05 2022
05 2022
Historique:
pubmed:
3
5
2022
medline:
31
5
2022
entrez:
2
5
2022
Statut:
ppublish
Résumé
Immune-related adverse events (irAEs) are caused by immune checkpoint inhibitors in several organs including the endocrine glands. Thyroid dysfunction (thyroid irAEs) is often observed among endocrine irAEs and is induced by blockade of programmed cell death 1 (PD-1), programmed death ligand 1, or PD-1 plus cytotoxic T-lymphocyte antigen 4. Endocrinologically, destructive thyroiditis or hypothyroidism is observed in most cases, whereas hyperthyroidism (Graves' disease) is rare. Most patients who develop destructive thyroiditis or hypothyroidism subsequently require thyroid hormone replacement therapy. Thyroid irAE development is associated with prolonged survival in patients with non-small cell lung carcinoma. The incidence of thyroid irAEs is higher in patients who are positive versus negative for anti-thyroid antibodies at baseline, suggesting that these antibodies can predict thyroid irAE development. Cytotoxic T cells, especially CD4 T cells, are reportedly involved in the development of destructive thyroiditis. In this review, we describe the clinical features, potential biomarkers, and mechanism of thyroid irAEs.
Identifiants
pubmed: 35501263
pii: S1521-690X(22)00047-1
doi: 10.1016/j.beem.2022.101660
pii:
doi:
Substances chimiques
Immune Checkpoint Inhibitors
0
Programmed Cell Death 1 Receptor
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
101660Informations de copyright
Copyright © 2022 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest S.I. received personal fees from Ono Pharmaceutical Co. Ltd., Japan, Bristol-Myers Squibb, Japan, Chugai Pharmaceutical Co., Ltd., Japan, MSD K.K., Japan, AstraZeneca Co., Ltd., Japan, and Merck Biopharma Co., Ltd., Japan outside of this study. H.A. received grants from Ono Pharmaceutical Co., Ltd., MSD K.K., and Chugai Pharmaceutical Co., Ltd., and personal fees from Ono Pharmaceutical Co., Ltd., Bristol-Myers Squibb, and MSD K.K. outside of this study. The remaining authors have nothing to disclose.