Reduced Tumor Size of Untreated Papillary Thyroid Carcinoma After Immune Checkpoint Inhibitor–Induced Thyroiditis

Dennis H. Chen, MD; Heinz-Josef Lenz, MD; Melissa G. Lechner, MD/PhD; Trevor E. Angell, MD

AACE Clinical Case Reports (Sep 2023)

Reduced Tumor Size of Untreated Papillary Thyroid Carcinoma After Immune Checkpoint Inhibitor–Induced Thyroiditis

Dennis H. Chen, MD,
Heinz-Josef Lenz, MD,
Melissa G. Lechner, MD/PhD,
Trevor E. Angell, MD

Affiliations

Dennis H. Chen, MD: Department of Medicine, Keck School of Medicine of University of Southern California, Los Angeles, California
Heinz-Josef Lenz, MD: Division of Oncology, Norris Comprehensive Cancer Center and Keck School of Medicine of University of Southern California, Los Angeles, California
Melissa G. Lechner, MD/PhD: Division of Endocrinology, Diabetes and Metabolism, David Geffen School of Medicine, University of California, Los Angeles, California
Trevor E. Angell, MD: Division of Endocrinology and Diabetes, Keck School of Medicine of University of Southern California, Los Angeles, California; Address correspondence to Dr Trevor E. Angell, Division of Endocrinology and Diabetes, Keck School of Medicine of University of Southern California, 2020 Zonal Avenue, IRD 620, Los Angeles, CA 90089.

Journal volume & issue: Vol. 9, no. 5
pp. 162 – 165

Abstract

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Background/Objective: Immune checkpoint inhibitors (CPIs) activate antitumoral immune responses and are used to treat multiple types of primary and metastatic malignancies. Thyroid dysfunction is a known immune-related adverse event of CPI therapy. There are few data on the effect of CPI and CPI-induced thyroiditis on primary papillary thyroid carcinoma (PTC). We present a patient who developed CPI-induced thyroiditis during treatment for a nonthyroid malignancy and subsequent regression of a coexisting untreated primary PTC. Case Report: A 49-year-old man with metastatic colon adenocarcinoma was found to have a large right thyroid nodule with biopsy confirmation of PTC. He did not have compressive symptoms or evidence of metastatic PTC. Resection was not performed because of colon cancer therapy. Treatment with CPI (ezabenlimab, an anti–programmed cell death protein 1 antibody) was initiated for the treatment of colon cancer. Four months after the initiation of CPI therapy, testing showed thyroid–stimulating hormone and free thyroxine levels of 174.9 (0.3-4.0 mIU/L) and 0.67 (0.93-1.70 ng/dL), respectively, consistent with CPI-induced hypothyroidism. Levothyroxine therapy was initiated. Repeat imaging 3 months later demonstrated a decrease in the tumor size to 4.1 × 4.9 × 4.2 cm (calculated volume change, −8.3% from baseline). At the last imaging, 1 year after the onset of CPI-induced thyroiditis, the PTC continued to decrease in size and measured 2.9 × 3.9 × 3.2 cm (volume change, −60.7% from baseline). Discussion: CPI-induced thyroiditis suggests the development of an immune response against thyroid tissue and may reflect a similar increased immune response against PTC cells leading to tumor regression in this case. Conclusion: Further research to assess the immunologic mechanism underlying this association is warranted to potentially develop improved immunotherapy for PTC.

Published in AACE Clinical Case Reports

ISSN: 2376-0605 (Online)
Publisher: Elsevier
Country of publisher: United States
LCC subjects: Medicine: Internal medicine: Specialties of internal medicine: Diseases of the endocrine glands. Clinical endocrinology
Website: https://www.journals.elsevier.com/aace-clinical-case-reports

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