Chronic inflammatory demyelinating polyneuropathy associated with tumor necrosis factor-alpha antagonists.
Biologic therapy with tumor necrosis factor (TNF)-alpha 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-alpha 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-alpha 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-alpha antagonists. IVIg may reverse and stabilize the inflammatory process.
Alshekhlee
Amer
A
The Neurological Institute, University Hospitals Case Medical Center, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, Ohio 44106-5040, USA. amer.alshekhlee@uhhospitals.org
Basiri
Kevian
K
Miles
J Douglas
JD
Ahmad
Saef A
SA
Katirji
Bashar
B
D000911:Antibodies, Monoclonal / Q000009:adverse effects; D018501:Antirheumatic Agents / Q000009:adverse effects*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D004568:Electrodiagnosis; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage; D007165:Immunosuppression Therapy / Q000009:adverse effects / Q000379:methods; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D018908:Muscle Weakness / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology; D009431:Neural Conduction / Q000187:drug effects / Q000276:immunology; D010146:Pain / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology; D020335:Paraparesis / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology; D010525:Peripheral Nerves / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D020277:Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / Q000139:chemically induced* / Q000276:immunology / Q000503:physiopathology; D018124:Receptors, Tumor Necrosis Factor; D020127:Recovery of Function / Q000187:drug effects / Q000276:immunology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000378:metabolism
D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D016756:Immunoglobulins, Intravenous; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept