Adalimumab-Induced CIDP in a Patient With Inflammatory Bowel Disease

Introduction: The increasing utilization of biologic agents in the management of medical conditions has raised significant concerns regarding potential adverse events, including the risk of Acute Inflammatory Demyelinating Polyneuropathy (AIDP) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP).
Inflammatory bowel disease (IBD) is an independent risk factor for the development of CIDP, with rare associations with TNF-α inhibitors (TNFis) in less than 1% of cases.


Description: A 27-year-old female with a history of Crohn's disease, who had been receiving Adalimumab, presented with two weeks of muscle weakness and paraesthesia. She was initially diagnosed with acral dysethesia. Her condition progressively deteriorated, leading to impaired ambulation, severe dysphagia, and dysphonia. Neurological examination revealed generalized areflexia. Both the MRH and cervical spine MRI were unremarkable. Lumbar punctures showed elevated protein, but were traumatic, precluding cell count. Notably, elevated GM1 ganglioside antibodies were detected. Lumbar spine MRI illustrated nerve root enhancement, suggestive of Guillain-Barré syndrome (GBS). Nerve conduction studies confirmed an early AIDP. The patient received five days of intravenous immunoglobulin (IVIG) with partial recovery.
Six months later, the patient had not returned to her pre-illness physical baseline. A repeat electromyography (EMG) indicated motor axonal and demyelinating peripheral polyneuropathy.


Discussion: This case highlights the critical ramifications of biologically induced neurotoxicity. Despite its rarity, AIDP and CIDP must be considered in patients presenting with progressive neurological symptoms while undergoing TNF-α inhibitor therapy. Adalimumab may precipitate AIDP by disrupting TNF's immunoregulatory functions, impairing the apoptosis of autoreactive T cells, and altering cytokine profiles (reducing IL-10 and increasing IL-12). This dysregulation may prolong myelin-targeting immune responses, facilitating demyelination.
Extended follow-up after diagnosing Adalimumab-induced AIDP is critical, as additional therapy such as steroids, IVIG, and therapeutic plasma exchange may be necessary. As the medical community increasingly adopts these treatments, it is imperative to maintain vigilance regarding their safety profiles.