Format

Send to

Choose Destination
Endocr Pathol. 2019 Jun;30(2):163-167. doi: 10.1007/s12022-019-9579-2.

Pembrolizumab-Induced Thyroiditis.

Author information

1
Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Six Founders Pavilion, Philadelphia, PA, 19104-4283, USA. Brittney.imblum@uphs.upenn.edu.
2
Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania, 3400 Spruce Street, Six Founders Pavilion, Philadelphia, PA, 19104-4283, USA.
3
Department of Surgery and Division of Endocrine & Oncologic Surgery, Hospital of the University of Pennsylvania, 3400 Spruce Street, Four Silverstein, Philadelphia, PA, 19104-4283, USA.

Abstract

Immune checkpoint inhibitors act to restore T cell-mediated antitumor immunity. By this nature, these cancer immunotherapy drugs are associated with various immune-related adverse events such as thyroid dysfunction. We describe a case of thyrotoxicosis secondary to a programmed cell death 1 (PD-1) immune checkpoint inhibitor, pembrolizumab. A 30-year-old female was started on pembrolizumab immunotherapy for stage III small cell carcinoma of the ovary, hypercalcemic type. Thirteen days after her second cycle of therapy, she presented with symptoms consistent with thyrotoxicosis. A thyroiditis was diagnosed by thyroid function tests and ultrasonography. She was originally treated with prednisone and metoprolol for possible Grave's disease. Pertechnetate thyroid scan was more consistent with thyroiditis secondary to pembrolizumab. She underwent a total thyroidectomy 10 days after initial presentation for refractory thyrotoxicosis despite maximal medical therapy. Her symptoms resolved and thyroid function tests significantly improved. Pathology was consistent with severe thyroiditis. Immune microenvironment may play a role in the expression of programmed cell death protein 1 ligand 1 (PD-L1). Chronic inflammation surrounding tumor upregulates PD-L1 expression on tumor cells by the release of cytokines, which acts to inhibit tumor destruction. We suggest that our patient had an undetected chronic inflammation of the thyroid, specifically Hashimoto's thyroidits, which predisposed her to thyroid destruction when taking pembrolizumab. Understanding that an inflammatory environment impacts thyroid toxicity to PD-1 inhibitor therapy is novel and should be further studied.

KEYWORDS:

PD-1 inhibitor; PDL-1 inhibitor; Pembrolizumab; Small cell carcinoma of ovary; Thyroid; Thyroiditis; Thyrotoxicosis

PMID:
31111437
DOI:
10.1007/s12022-019-9579-2

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center