Guillain-Barré Syndrome in a Patient Receiving Anti-Tumor Necrosis Factor for Crohn Disease: Coincidence or Consequence?

• Published in: The American journal of case reports 2024-06, Vol.25, p.e943709-e943709-5
• Main Authors: Ferreira, Sandro da Costa, Vasconcelos, Juarez Roberto de Oliveira, Rezende, Rosamar Eulira Fontes, Aprile, Lilian Rose Otoboni, Troncon, Luiz Ernesto de Almeida
• Format: Article
• Language: English
• Subjects: Crohn Disease - complications; Crohn Disease - drug therapy; Female; Guillain-Barre Syndrome - chemically induced; Guillain-Barre Syndrome - diagnosis; Humans; Infliximab - adverse effects; Infliximab - therapeutic use; Middle Aged; Tumor Necrosis Factor-alpha - antagonists & inhibitors
• ISSN: 1941-5923; 1941-5923
• 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.