Guillain-barre syndrome developing during ınfliximab treatment for psoriatic arthritis: a case report

Abstract

Tumor necrosis factor (TNF)-α plays an important role in many aspects of immune system development, immune-response regulation, and T-cell–mediated tissue injury. The evidence that TNF-α, released by auto reactive T cells and macrophages, may contribute to the pathogenesis of immune-mediated demyelinating neuropathies is reviewed. Demyelinating neuropathies are rare adverse events of anti–TNF-α therapy. Improvement usually occurs after drug interruption and/or in association with conventional treatments for demyelinating neuropathies. We aimed to report a patient with demyelinating neuropathy occurring after TNF blocker (infliximab) treatment. The development of Guillain-Barre syndrome in this report may have been secondary to anti-TNF-α treatment. The influence of anti TNF-α treatment continuation on the long-term course of neuropathy is variable, suggesting that anti-TNF-α treatment withdrawal is not always necessary for neuropathy control. But such as the report, anti-TNF-α treatment may be stopped.

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