背景:由抗PD-1免疫剂引起的继发性肾上腺功能不全的不良事件在临床实践中相对罕见,所以在这篇文章中,我们回顾性分析了3例因tislelizumab免疫治疗非小细胞肺癌(NSCLC)导致继发性肾上腺皮质功能障碍的患者,并回顾了文献.通过总结患者的临床特征来调查这种罕见的免疫相关不良事件。
方法:我们报告了2021年7月至2023年10月在我们医院接受tislelizumab免疫疗法诱导的继发性肾上腺皮质功能障碍的3例NSCLC患者。我们分析和总结了临床特点,实验室检查,病理分期,等。我们还回顾了免疫治疗引起的垂体炎症和肾上腺皮质功能障碍的相关文献。
结果:3名患者的中位年龄为56岁。所有患者均有吸烟史。接受tislelizumab治疗后(中位周期:7),实验室检查显示早晨皮质醇和促肾上腺皮质激素(ACTH)减少,两者均被诊断为继发性肾上腺功能不全.只有一名患者出现疲劳症状,呕吐,和减肥。其中一名患者同时患有亚临床甲状腺功能减退症。所有3例患者均停止免疫治疗并接受糖皮质激素替代治疗。在最后一次随访中,三个病人都没有重新开始免疫治疗,因为皮质醇没有恢复正常.这与以前的报告相似。
结论:根据以前的报告和我们的三个案例,当接受免疫治疗的NSCLC患者的实验室检查显示早晨皮质醇和ACTH水平降低时,特别是当临床症状明显时,应考虑免疫治疗相关垂体炎症引起继发性肾上腺皮质功能障碍的可能性.应提供及时的监测和激素替代疗法,以防止肾上腺危机。
BACKGROUND: Adverse events of secondary adrenal insufficiency caused by anti-PD-1 immune agents are relatively rare in clinical practice, so in this article, we retrospectively analyzed three patients who suffered secondary adrenal cortex dysfunction caused by tislelizumab immunotherapy for Non-Small Cell Lung Cancer (NSCLC)and reviewed the literature. This rare immune-related adverse event was investigated by summarizing the clinical features of the patients.
METHODS: We reported three NSCLC patients who suffered secondary adrenal cortex dysfunction induced by tislelizumab immunotherapy at our hospital from July 2021 to October 2023. We analyzed and summarized the clinical characteristic, laboratory examination, pathological staging, etc. We also reviewed related literature of pituitary inflammation and adrenal cortex dysfunction caused by immunotherapy.
RESULTS: The median age of the three patients was 56 years. All the patients had a history of smoking. After receiving tislelizumab treatment (median cycle: 7), laboratory examination showed a decrease in morning cortisol and adrenocorticotropic hormone (ACTH), both were diagnosed with secondary adrenal insufficiency. Only one patient had symptoms of fatigue, vomiting, and weight loss. One of these patients also had simultaneous subclinical hypothyroidism. All three patients discontinued immunotherapy and received replacement therapy with glucocorticoids. At the last follow-up, none of the three patients restarted immunotherapy, because cortisol did not return to normal. This is similar to that of previous reports.
CONCLUSIONS: Based on previous reports and our three cases, when laboratory tests of NSCLC patients receiving immunotherapy showed a decrease in morning cortisol and ACTH levels, especially when clinical symptoms were obvious, the possibility of immunotherapy-related pituitary inflammation causing secondary adrenal cortex dysfunction should be considered. Prompt monitoring and hormone replacement therapy should be provided to prevent adrenal crises.