Exp Clin Endocrinol Diabetes 2017; 125(04): 267-269
DOI: 10.1055/s-0042-119528
Letter to the Editor
© Georg Thieme Verlag KG Stuttgart · New York

Hypothyroidism in Cancer Patients on Immune Checkpoint Inhibitors with anti-PD1 Agents: Insights on Underlying Mechanisms

M. Alhusseini
1   Division of Endocrinology, University Health Center, Wayne State University School of Medicine, Detroit, USA
,
J. Samantray
1   Division of Endocrinology, University Health Center, Wayne State University School of Medicine, Detroit, USA
› Author Affiliations
Further Information

Publication History

received 15 July 2016
first decision 27 August 2016

accepted 21 October 2016

Publication Date:
10 January 2017 (online)

Abstract

Background: Immune therapy using monoclonal antibodies against cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and programmed cell death 1 receptor (PD-1) for various cancers have been reported to cause thyroid dysfunction. Little is known, however, about the underlying pathogenic mechanisms and the course of hypothyroidism that subsequently develops. In this report, we use the change in thyroglobulin and thyroid antibody levels in patients on immune therapy who develop hypothyroidism to better understand its pathogenesis as well as examine the status of hypothyroidism in the long term.

Methods: We report a case series of 10 patients who developed hypothyroidism after initiation of immune therapy (either anti-PD-1 alone or in combination with anti-CTLA-4). Available thyroid antibodies including anti-thyroglobulin (anti-Tg), anti-thyroid peroxidase (anti-TPO), and thyroid stimulating immunoglobulin (TSI) were noted during the initial thyroiditis phase as well as the hypothyroid phase. Persistence or remission of hypothyroidism was noted at 6 months.

Summary: During the thyroiditis phase, 50% of the patients had elevated Tg titers, 40% had elevated anti-Tg, and 40% had elevated TSI. All of these titers decreased during the hypothyroid phase. Permanent hypothyroidism was noted in 80% of the cases.

Conclusion: Hypothyroidism following initiation of immune therapy has immunologic and non-immunologic mediated mechanisms and is likely to be persistent.

 
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