Annals of Neurology · 1986 · 113 citations · 24 references
Life SciencesImmunologyNeurologyAutoimmunityClinical ImmunologyNeuroimmunologyAntibody CharacterizationAutoantibodiesAutoimmune Neurological DisordersDiagnostic ImmunologyHumoral ImmunityPeripheral Nervous System ImmunityAntibody Titer AnalysisAntibody Titer DeclineAntibody Titer KineticsGuillain-barré Syndrome PathogenesisMyelin Antigen AutoimmunityMyelin AntigensPeripheral Nerve AutoimmunityPeripheral Nervous System Myelin
Anti-peripheral-nerve myelin antibodies (anti-PNM Ab) can be detected in the serum of all patients with acute-phase Guillain-Barré syndrome (GBS) thus far tested. Correlation of the titer of this antibody with the clinical course would help to establish a role for the humoral immune system in the pathophysiology of GBS. In this study, anti-PNM Ab levels were measured in serial serum samples of 7 patients with GBS with an assay that detects antibodies bound to peripheral nerve myelin antigens by fixation of the first component of complement. Although the titers of anti-PNM Ab detected in these patients varied between 0 and 256 U/ml, the antibody titer was always highest on admission (35 to 256 U/ml) and rapidly declined during a one-to-three-week period. Disappearance of antibodies or very low levels of them correlated with cessation of progression and considerable clinical improvement as documented by increased pulmonary vital capacity and muscular strength. Low but measurable antibody titers (5 to 12 U/ml) were frequently found up to four months following the acute neurological deficit. The close temporal relationship between anti-PNM Ab titer and the clinical course in GBS suggests that antibody most likely participates through complement activation in peripheral nerve demyelination.
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Plasmapheresis and acute Guillain‐Barre syndrome
Neurology · 1985 · 772 citations
Journal of Allergy · 1949 · 358 citations