目的:报道1例使用阿达木单抗后出现变异型吉兰巴雷综合征(Gillain-Barr é syndrome, GBS)——Miller- Fisher综合征(Miller-Fisher syndrome, MFS)患者的临床资料,为更一步阐明肿瘤坏死因子-α (tumor necrosis factor-α ,TNF-α)抑制剂与GBS的相关性提供新的理论依据。

方法:报道1例克罗恩病患者使用阿达木单抗后出现MFS,包括临床表现、辅助检查、影像学检查和诊治过程等,并结合文献，分析此病例可能的发病机制。

结果:男性患者,32岁,3年前确诊克罗恩病,使用英夫利西单抗3年,后转用阿达木单抗4月余。于末次使用阿达木单抗10d后，以"双眼视物成双6d"入院。查体显示双眼活动受限，头颅MRI平扫及增强扫描未见异常，血清及脑脊液周围神经病抗体谱检测提示血清抗GT1a抗体lgG阳性、抗GQ1b抗体lgG阳性。患者被诊断为GBS亚型的MFS,停用阿达木单抗，静脉注射人免疫球蛋白(intravenous immunoglobin, IMIG)冲击治疗，辅以维生素B₁₂、维生素B₁,治疗,症状好转出院。

结论:阿达木单抗可能引起GBS,但其机制仍没有阐明。临床上，需关注应用单克隆抗体治疗时,可能增加周围神经性疾病的发病风险。

Objective: To report the clinical data of a patient who developed Miller-Fisher syndrome (MFS), the variant type of Guillain-Barré syndrome (GBS) after the administration of adalimumab, which aims to provide novel evidence of the association between TNF-α inhibitor and GBS.

Methods: We reported a case of MFS in a Crohn's disease patient following adalimumab administration. The clinical manifestations, auxiliary examinations, radiological scans, and diagnostic and treatment procedures were stated. Furthermore, the possible pathogenesis was assessed by reviewing the relevant references.

Results: A male patient aged 32 years old was diagnosed as Crohn 's disease three years ago. He was treated with infliximab for three years before switching to adalimumab for over four months. Ten days after his last dose of adalimumab, he complained of " double visions for 6 days" and was admitted to the hospital. On examination, there was limited movement in both eyes, and no abnormality was seen on brain MRI scanning with or without enhancement. The autoantibodies (anti-GT1a IgG antibody and anti-GQ1b IgG antibody) were positive in his blood test. He was diagnosed as MFS, which is a variant type of GBS. After discontinuing adalimumab, he was treated with intravenous immunoglobin, vitamin B₁₂, and vitamin B₁. His symptoms improved and he was discharged.

Conclusion:GBS can be caused by adalimumab, but the mechanism should be further investigated. Clinically, more attention should be paid to the possible increased risk of developing peripheral neuropathies when monoclonal antibody therapy is applied.