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Chronic inflammatory demyelinating polyneuropathy associated with tumor necrosis factor‐α antagonists
Author(s) -
Alshekhlee Amer,
Basiri Kevian,
Miles J. Douglas,
Ahmad Saef A.,
Katirji Bashar
Publication year - 2010
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21584
Subject(s) - medicine , chronic inflammatory demyelinating polyneuropathy , etanercept , rheumatoid arthritis , discontinuation , infliximab , tumor necrosis factor alpha , gastroenterology , polyneuropathy , intravenous immunoglobulin therapy , surgery , immunology , antibody
Biologic therapy with tumor necrosis factor (TNF)‐α antagonists for rheumatoid arthritis has been well established. We describe two patients with rheumatoid arthritis who developed chronic inflammatory demyelinating polyneuropathy (CIDP) during their course of therapy with TNF‐α antagonists. A 45‐year‐old woman and a 49‐year‐old man, both with a history of rheumatoid arthritis, were treated with etanercept and infliximab, respectively. Clinical signs of peripheral neuropathy developed 2 weeks and 12 months after the initiation of TNF‐α antagonists. Electrodiagnostic studies at variable points during the disease course showed signs of acquired demyelination consistent with CIDP. Cerebrospinal fluid examination showed albuminocytologic dissociation (total protein concentration 118 mg/dl and 152 mg/dl, respectively). Both patients failed to improve after discontinuation of the offending agent, and they responded poorly to corticosteroids. However, there was clinical and electrophysiologic recovery after initiation of intravenous immunoglobulin (IVIg) therapy. CIDP may occur early or late during the treatment course with TNF‐α antagonists. IVIg may reverse and stabilize the inflammatory process. Muscle Nerve 41: 742–747, 2010