Inflammatory bowel disease therapies and demyelinating diseases: a practical guide to therapeutic benefit and risk

TL;DR

This paper reviews how IBD treatments may affect patients with or at risk for demyelinating diseases like MS, offering guidance for managing both conditions.

Contribution

A practical framework for clinicians to manage IBD therapies in patients with coexisting demyelinating diseases is proposed.

Findings

Anti-tumor necrosis factor agents are linked to new-onset or worsening demyelinating events.

Some IBD therapies like sphingosine-1-phosphate receptor modulators are used for both IBD and MS.

Multidisciplinary collaboration and early symptom recognition are critical for optimizing outcomes.

Abstract

Demyelinating diseases, particularly multiple sclerosis (MS), present a unique therapeutic challenge in the management of inflammatory bowel disease (IBD). Although rare, the co-occurrence of IBD and demyelinating disorders is well-documented and may reflect shared immune, genetic, and environmental risk factors. As the therapeutic landscape of IBD expands to include biologics and small molecules that target immune pathways also implicated in MS, concerns around neurological safety have grown. In particular, anti-tumor necrosis factor agents have been consistently linked to new-onset or worsening demyelinating events, while other treatments such as sphingosine-1-phosphate receptor modulators and natali­zumab are licensed for both IBD and MS, though real-world data in patients with coexisting disease remain limited. This review synthesizes current evidence regarding the neurological safety and efficacy of IBD therapies in the context of demyelinating disease. It proposes a practical framework for clinicians, addressing management strategies for patients with confirmed MS, those at increased risk, and individuals who develop neurological symptoms during treatment. In the absence of formal guidelines, multidisciplinary collaboration, early recognition of symptoms, and careful treatment selection are important to optimize both gastrointestinal and neurological outcomes.

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