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in chronic inflammatory demyelinating polyneuropathy
From the Department of Neurology, Chiba University School of Medicine, Japan.
Address correspondence and reprint requests to Dr. S. Kuwabara, Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; e-mail: kwbr{at}mb.infoweb.ne.jp
BACKGROUND: Activated macrophages and T lymphocytes may play a role in the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP). Both cell types secrete tumor necrosis factor-
(TNF), which has toxic effects on myelin and endothelial cells.
METHODS: The serum concentration of TNF was measured by ELISA and compared with clinical and electrophysiological profiles in 20 patients with CIDP.
RESULTS: An increased serum level of TNF was detected in 5 (25%) patients and was associated with subacute progression, severe neurologic disabilities, and symmetric weakness involving proximal as well as distal muscles. TNF levels increased during the active phase in this subgroup of patients. The levels of TNF correlated with the severity of demyelinating conduction abnormalities in the intermediate as well as distal nerve segments, suggesting demyelination diffusely distributed along the nerves.
CONCLUSION: Circulating TNF increases during the active phase in a subgroup of CIDP patients and may play a role in the pathogenesis of demyelination and the breakdown of the blood–nerve barrier in CIDP.
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