Immune checkpoint inhibitor-related thyroid dysfunction.


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
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

101660

Informations 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.

Auteurs

Shintaro Iwama (S)

Department of Endocrinology and Diabetes, Nagoya University Hospital, Japan. Electronic address: siwama@med.nagoya-u.ac.jp.

Tomoko Kobayashi (T)

Department of Endocrinology and Diabetes, Nagoya University Hospital, Japan.

Yoshinori Yasuda (Y)

Department of Endocrinology and Diabetes, Nagoya University Hospital, Japan.

Hiroshi Arima (H)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, Japan.

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Classifications MeSH