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

Q3 Medicine
Dennis H. Chen MD , Heinz-Josef Lenz MD , Melissa G. Lechner MD/PhD , Trevor E. Angell MD
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引用次数: 2

Abstract

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.

免疫检查点抑制剂诱导甲状腺炎后未治疗甲状腺乳头状癌的肿瘤缩小。
背景/目的:免疫检查点抑制剂(CPIs)可激活抗肿瘤免疫反应,用于治疗多种原发性和转移性恶性肿瘤。甲状腺功能障碍是已知的CPI治疗的免疫相关不良事件。关于CPI和CPI诱导的甲状腺炎对原发性乳头状甲状腺癌(PTC)的影响,目前尚无相关数据。我们报告了一名患者,他在非甲状腺恶性肿瘤的治疗过程中发生了CPI诱导的甲状腺炎,随后并发未经治疗的原发性PTC消退。病例报告:一名49岁的转移性结肠腺癌患者被发现有一个巨大的右甲状腺结节,活检证实为PTC。他没有压迫性症状,也没有转移性PTC的证据。因结肠癌癌症治疗而未进行切除手术。开始用CPI(ezabenlimab,一种抗程序性细胞死亡蛋白1抗体)治疗结肠癌。CPI治疗开始四个月后,测试显示促甲状腺激素和游离甲状腺素水平分别为174.9(0.3-4.0 mIU/L)和0.67(0.93-1.70 ng/dL),与CPI诱导的甲状腺功能减退一致。开始使用左旋甲状腺素治疗。3个月后的重复成像显示肿瘤大小减小到4.1×4.9×4.2厘米(计算体积变化,与基线相比为-8.3%)。在CPI诱导的甲状腺炎发作1年后的最后一次成像中,PTC的大小继续减小,测量值为2.9×3.9×3.2cm(体积变化,比基线变化-60.7%)。讨论:CPI诱导的甲状腺炎表明对甲状腺组织产生了免疫反应,并可能反映出对PTC细胞的类似免疫反应增加,导致这种情况下的肿瘤消退。结论:有必要进一步研究评估这种关联的免疫机制,以开发潜在的改进PTC免疫疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
AACE Clinical Case Reports
AACE Clinical Case Reports Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
2.30
自引率
0.00%
发文量
61
审稿时长
55 days
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