Autor(es): Sharief M K,Ingram D A,Swash M

Resumo: Autoimmune damage to peripheral nerves, mediated by activated T lymphocytes and macrophages, underlies the pathogenesis of inflammatory demyelination in Guillain-Barré syndrome. Both T lymphocytes and macrophages secrete tumor necrosis factor-alpha, a cytokine that exerts toxic effects on myelin, Schwann cells, and endothelial cells. The reportedly high serum levels of this cytokine in patients with Guillain-Barré syndrome may reflect the degree of immune activation rather than a direct pathogenic effect. We compared serum levels of tumor necrosis factor-alpha, interleukin-1 beta, and soluble interleukin-2 receptor with well-established electrodiagnostic criteria for primary demyelination in 23 patients with Guillain-Barré syndrome, to assess the relationship between these cytokines and peripheral myelin damage. High serum levels of tumor necrosis factor-alpha were associated with prolonged distal motor latencies and slowed motor conduction velocities, prolonged or absent F-wave responses, and reduced amplitude of distal compound muscle action potentials. No significant correlation was observed between electrodiagnostic criteria for primary demyelination and serum levels of interleukin-1 beta or soluble interleukin-2 receptor. These findings suggest a putative role of tumor necrosis factor-alpha in the pathogenesis of peripheral nerve demyelination in Guillain-Barré syndrome.

Imprenta: Annals of Neurology, v. 42, n. 1, p. 68-73, 1997

Identificador do objeto digital: 10.1002/ana.410420112

Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Cytokines

Data de publicação: 1997

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