S4936 Beyond the Gut: TNF-Alpha Inhibitor-Induced Demyelinating Neuropathy and Bladder Dysfunction in a Crohn’s Disease Patient With Negative MRI Findings

Introduction: Tumor necrosis factor-alpha (TNF-α) inhibitors are a cornerstone in managing inflammatory bowel disease. Among them, infliximab-a chimeric monoclonal IgG antibody-has the highest reported incidence of neurological adverse events, including peripheral neuropathy. We report a rare case of infliximab-associated demyelinating neuropathy presenting as urinary incontinence and motor dysfunction, expanding the neurological spectrum of TNF-α inhibitor complications. Case Description/Methods: A 25-year-old woman presented with a 7-month history of abdominal pain and diarrhea. Stool calprotectin was >1000 µg/g, and colon biopsy confirmed Crohn’s disease with transmural pancolitis and noncaseating granulomas. She was initially treated with dexamethasone and azathioprine with partial symptom control. Subcutaneous infliximab was initiated, improving gastrointestinal symptoms. However, post-induction, she developed urinary leakage, reduced urine stream, pelvic weakness, difficulty walking, and impaired grip. Physical exam showed right lower limb weakness (4+/5), upgoing plantar response, hyperreflexia, rigidity, and jerky movements. Sensory loss followed a stocking distribution. Urodynamic studies and urethral pressure profilometry indicated neurogenic bladder with low detrusor pressure, reduced flow rate, and intermittent low urethral occlusion pressure. Nerve conduction studies revealed diminished F-wave responses and compound muscle action potential amplitude; electromyography showed mild neurogenic changes. Brain and spine magnetic resonance imaging were negative for central demyelination. Initial management targeted presumed urologic dysfunction, but poor response led to suspicion of infliximab-induced neuropathy. Infliximab was discontinued, and high-dose dexamethasone was initiated, leading to rapid improvement and suggesting an immune-mediated process. After a 3-month steroid taper, she had improved urinary symptoms, with mild residual limb weakness and occasional leakage. Discussion: Neurological complications of TNF-α inhibitors are rare but clinically significant. This case is unique in that urinary incontinence and pelvic dysfunction were the first manifestations of infliximab-induced demyelinating neuropathy. New-onset urinary or motor symptoms in young patients should prompt early neurologic evaluation and discontinuation of the agent, even with a normal magnetic resonance imaging. A delayed diagnosis may result in irreversible deficits.

Authors

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001147204.37373.19
Primary Topic
Peripheral Neuropathies and Disorders
Type
article
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article

S4936 Beyond the Gut: TNF-Alpha Inhibitor-Induced Demyelinating Neuropathy and Bladder Dysfunction in a Crohn’s Disease Patient With Negative MRI Findings

Shaaf Ahmad, Ghias Un Nabi Tayyab, Ayesha Siddiqua, Jazza Jamil
The American Journal of Gastroenterology
Peripheral Neuropathies and Disorders
article

S4936 Beyond the Gut: TNF-Alpha Inhibitor-Induced Demyelinating Neuropathy and Bladder Dysfunction in a Crohn’s Disease Patient With Negative MRI Findings

Shaaf Ahmad, Ghias Un Nabi Tayyab, Ayesha Siddiqua, Jazza Jamil
article en

Abstract

Introduction: Tumor necrosis factor-alpha (TNF-α) inhibitors are a cornerstone in managing inflammatory bowel disease. Among them, infliximab-a chimeric monoclonal IgG antibody-has the highest reported incidence of neurological adverse events, including peripheral neuropathy. We report a rare case of infliximab-associated demyelinating neuropathy presenting as urinary incontinence and motor dysfunction, expanding the neurological spectrum of TNF-α inhibitor complications. Case Description/Methods: A 25-year-old woman presented with a 7-month history of abdominal pain and diarrhea. Stool calprotectin was >1000 µg/g, and colon biopsy confirmed Crohn’s disease with transmural pancolitis and noncaseating granulomas. She was initially treated with dexamethasone and azathioprine with partial symptom control. Subcutaneous infliximab was initiated, improving gastrointestinal symptoms. However, post-induction, she developed urinary leakage, reduced urine stream, pelvic weakness, difficulty walking, and impaired grip. Physical exam showed right lower limb weakness (4+/5), upgoing plantar response, hyperreflexia, rigidity, and jerky movements. Sensory loss followed a stocking distribution. Urodynamic studies and urethral pressure profilometry indicated neurogenic bladder with low detrusor pressure, reduced flow rate, and intermittent low urethral occlusion pressure. Nerve conduction studies revealed diminished F-wave responses and compound muscle action potential amplitude; electromyography showed mild neurogenic changes. Brain and spine magnetic resonance imaging were negative for central demyelination. Initial management targeted presumed urologic dysfunction, but poor response led to suspicion of infliximab-induced neuropathy. Infliximab was discontinued, and high-dose dexamethasone was initiated, leading to rapid improvement and suggesting an immune-mediated process. After a 3-month steroid taper, she had improved urinary symptoms, with mild residual limb weakness and occasional leakage. Discussion: Neurological complications of TNF-α inhibitors are rare but clinically significant. This case is unique in that urinary incontinence and pelvic dysfunction were the first manifestations of infliximab-induced demyelinating neuropathy. New-onset urinary or motor symptoms in young patients should prompt early neurologic evaluation and discontinuation of the agent, even with a normal magnetic resonance imaging. A delayed diagnosis may result in irreversible deficits.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 46%
Peripheral Neuropathies and Disorders
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