程序性细胞死亡（PD）-1抑制剂通过增强抗肿瘤免疫反应，显着改善了癌症患者的预后。然而，PD-1 抑制剂与免疫相关不良事件有关，其中一些不良事件罕见且可能危及生命。迄今为止，尚未有新型PD-1抑制剂（信迪利单抗）诱发甲状腺功能减退症引起肌酸激酶（CK）和肌酐升高的报道。 一名63岁男性食管癌患者出现甲状腺功能减退症，并伴有不明原因的肌酐升高。信迪利单抗治疗后的CK和肌酐。由于CK和肌酐的升高与甲状腺素的降低平行，在排除其他潜在情况后，我们推测肌肉和肾功能障碍可能是由信迪利单抗引起的甲状腺功能减退症引起的。随着患者甲状腺功能的改善，左旋甲状腺素替代治疗后，CK和肌酐水平同时恢复正常。该患者的CK和肌酐水平升高是由信迪利单抗引起的甲状腺功能减退症引起的。我们的案例强调了当患者出现无法解释的 CK 和肌酐水平升高时，牢记 PD-1 诱发的甲状腺功能减退症的重要性。甲状腺功能减退相关的肌肉和肾功能障碍可以通过甲状腺激素替代来恢复，需要及早发现并及时治疗，以避免这些患者不必要的检查和治疗。版权所有 © 2024 作者。由 Wolters Kluwer Health, Inc. 出版

Programmed cell death (PD) -1 inhibitors has significantly improved the prognosis of cancer patients by enhancing antitumor immune responses. However, PD-1 inhibitors are associated with immune-related adverse events, some of which are rare and potentially life-threatening. Thus far, elevated creatine kinase (CK) and creatinine caused by a novel PD-1 inhibitor (sintilimab)-induced hypothyroidism has not yet been reported.A 63-year-old male patient with esophageal cancer who developed hypothyroidism accompanied by unexplained increases in CK and creatinine after sintilimab treatment.Since the increases in CK and creatinine paralleled the decrease in thyroxine, after excluding other potential conditions, we speculated that the muscular and renal dysfunction might be caused by sintilimab-induced hypothyroidism.As the patient's thyroid function improved with levothyroxine replacement therapy, the levels of CK and creatinine concomitantly returned to normal.The elevated CK and creatinine levels in this patient were caused by sintilimab-induced hypothyroidism. Our case highlights the importance of keeping PD-1 induced hypothyroidism in mind when patients present with unexplained increased levels of CK and creatinine. Hypothyroidism-related muscular and renal dysfunctions, which can be restored with thyroid hormone replacement, need to be identified early and treated promptly so that unnecessary examinations and treatments can be avoided in these patients.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.