信迪利单抗致格林-巴利综合征1例临床分析

Clinical Analysis of Guillain-BarréSyndrome Induced by Sintilimab:A Case Report

目的探讨信迪利单抗致格林-巴利综合征(GBS)的临床特点、发病机制及诊治方案。方法回顾性分析1例应用信迪利单抗(2个周期)治疗原发性支气管肺癌诱发GBS的病例,并结合国家药品不良反应监测中心制定的不良反应关联性评价标准判断不良反应关联性,结合相关文献分析GBS的临床特点、发病机制、治疗方案等。结果该病例的GBS可能为信迪利单抗药品不良反应,常表现为无力、反射减弱(或消失)和感觉异常,对其行血浆置换术并予注射用甲泼尼龙琥珀酸钠(80 mg/160 mg)治疗,后转为口服甲泼尼龙片(60 mg),好转后减量续用。其发生机制可能为激活的外周组织中T淋巴细胞与外周神经元特异性作用导致的急性炎症性脱髓鞘性多发性神经病变。结论目前,国内有关信迪利单抗引起GBS的病例报道较少,其为该药罕见而严重的药品不良反应,一旦发生应首选大剂量糖皮质激素治疗,警惕治疗初期症状恶化,如无改善,可选用血浆置换或免疫球蛋白治疗。

Objective To investigate the clinical characteristics,pathogenesis and treatment scheme of Guillain-Barrésyndrome(GBS)induced by sintilimab.Methods A case with GBS induced by sintilimab in the treatment of primary bronchogenic carcinoma(two cycles)was analyzed retrospectively.The correlation of adverse drug reactions(ADRs)was evaluated according to the evaluation criteria for the correlation of ADRs formulated by the National Center for Adverse Drug Reaction Monitoring.The clinical characteristics,pathogenesis and treatment scheme of GBS were analyzed based on relevant studies.Results The GBS in this case might be an adverse reaction of sintilimab,and its clinical manifestations were weakness,reflex weakening(or disappearing)and sensory abnormality.The patient underwent plasma exchange and used Methylprednisolone Sodium Succinate for Injection(80 mg/160 mg).Later,he used Methylprednisolone Tablets orally(60 mg)instead of the above injection,and continued to use this drug with reduced doses after improvement.The pathogenesis of GBS might be acute inflammatory demyelinating polyneuropathy induced by specific effects between activated T lymphocytes and peripheral neurons in peripheral tissue.Conclusion Currently,there are a few case reports of GBS induced by sintilimab in China,and it is a rare and serious ADR of the drug.Once this ADR occurs,we should prioritize high-dose glucocorticoid,and be vigilant for worsening symptoms in the early stages of treatment.If there is no improvement,we can select plasma exchange or immunoglobulin.