Division of Gastroenterology, Department of Medicine, Hospital das Clínicas, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil.
Am J Case Rep. 2024 Jun 2;25:e943709. doi: 10.12659/AJCR.943709.
BACKGROUND Antibodies against tumor necrosis factor alpha (anti-TNF-alpha) are currently widely used in the treatment of inflammatory bowel diseases (IBD), despite a number of reported adverse effects. Diverse neurologic syndromes, including the Guillain-Barre syndrome (GBS), an immune-mediated disease characterized by evolving ascending limb weakness, sensory loss, and areflexia, have been described in association with anti-TNF-alpha therapy. CASE REPORT A 45-year-old White woman was in follow-up with fistulizing ileocolonic Crohn disease using combination therapy (infliximab plus azathioprine) as CD maintenance therapy. After 3 years of this immunosuppressive therapy, she presented with symmetrical and ascending paresis in the lower limbs, and later in the upper limbs, in addition to reduced reflexes in the knees, 1 day after an infliximab infusion. The patient was hospitalized and treatment for CD was suspended. Neurophysiology studies demonstrated a pattern compatible with acute inflammatory demyelinating polyradiculopathy, with predominantly motor involvement, consistent with Guillain-Barre syndrome (GBS). Clinical, laboratory, and imaging exams were unremarkable. She was treated with intravenous immunoglobulins, with a progressive and complete resolution of neurological symptoms. After 1-year follow-up, she presented with active Crohn disease, and we opted for treating her with vedolizumab, with which she achieved clinical and endoscopic remission. CONCLUSIONS Patients receiving biological therapy with anti-TNF-alpha agents should be monitored for central or peripheral neurological signs and symptoms. The development of GBS can be secondary to anti-TNF-alpha treatment. The positive temporal relationship with TNF-alpha therapy and onset of neurological symptoms reinforces this possibility.
尽管存在许多报道的不良反应,但肿瘤坏死因子-α(anti-TNF-α)抗体目前广泛用于治疗炎症性肠病(IBD)。与抗 TNF-α治疗相关,已描述了多种神经综合征,包括格林-巴利综合征(GBS),这是一种以进行性上升性肢体无力、感觉丧失和反射消失为特征的免疫介导性疾病。
一名 45 岁白人女性因瘘管性回肠结肠克罗恩病接受联合治疗(英夫利昔单抗加硫唑嘌呤)作为 CD 维持治疗。在接受这种免疫抑制治疗 3 年后,她在英夫利昔单抗输注后 1 天出现下肢对称和上升性无力,随后上肢也出现无力,且膝反射减弱。患者住院并暂停 CD 治疗。神经生理学研究表明,存在与急性炎症性脱髓鞘性多发性神经根病一致的模式,主要表现为运动受累,符合格林-巴利综合征(GBS)。临床、实验室和影像学检查无明显异常。她接受了静脉注射免疫球蛋白治疗,神经症状完全缓解。在 1 年随访时,她出现活动性克罗恩病,我们选择用维得利珠单抗治疗,她达到了临床和内镜缓解。
接受抗 TNF-α药物生物治疗的患者应监测中枢或周围神经系统体征和症状。GBS 的发生可能继发于抗 TNF-α治疗。与 TNF-α治疗和神经系统症状发作的时间相关性增强了这种可能性。