由sintilimab诱导的甲状腺功能低下引起的肌酸激酶和肌酸氨酸的可逆升高:一个病例报告
Shu-Rong Liu1, Zhen-Guang Zhao2, Rui-Ren Zhai1
1Department of Oncology, Sunshine Union Hospital, Weifang, Shandong Province, China.
Medicine
|October 21, 2024
概括
一种新型PD-1抑制剂sintilimab可以导致甲状腺功能低下,导致肌酸激酶 (CK) 和肌酸氨酸的升高. 早期诊断和甲状腺激素替代疗法可以恢复肌肉和功能,改善患者的治疗结果.
科学领域:
- 在瘤学瘤学.
- 免疫治疗是一种免疫疗法.
- 内分泌学 在内分泌学.
背景情况:
- 编程细胞死亡 (PD) -1 抑制剂增强抗瘤免疫力,但可能导致罕见的,严重的免疫相关不良事件.
- 辛提利马布是一种用于癌症治疗的新型PD-1抑制剂.
- 之前没有报告过因辛蒂利马布诱导的甲状腺功能低下而导致肌酸激酶 (CK) 和肌酸氨酸的升高.
研究的目的:
- 报告一种罕见的sintilimab诱导的甲状腺功能低下病例,其CK和肌素水平升高.
- 为了突出肌肉和功能障碍的潜力二次到PD-1抑制剂诱导的甲状腺功能低下症.
- 强调早期诊断和治疗这种不良事件的重要性.
主要方法:
- 一个63岁的男性食道癌患者的案例研究,该患者接受了sintilimab治疗.
- 监测甲状腺功能,CK和肌素水平.
- 排除其他可能导致CK和肌素升高的原因.
- 为甲状腺功能低下症开始的levothyroxine替代疗法.
主要成果:
- 患者在辛蒂利马布治疗后出现甲状腺功能低下症,同时CK和肌素的不明原因增加.
- 作为甲状腺功能的改善与levothyroxine治疗正常化CK和肌素水平.
- 这表明sintilimab诱导的甲状腺功能低下和肌肉/脏功能障碍之间存在因果关系.
结论:
- 辛提利马布诱导的甲状腺功能低下症可以表现为CK和肌素的升高,表明肌肉和功能障碍.
- 临床医生应考虑在癌症患者中考虑PD-1抑制剂诱导的甲状腺功能低下症,这些癌症患者的CK和肌氨酸含量不明原因增加.
- 及时的甲状腺激素替代对于恢复功能和避免不必要的调查至关重要.
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