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Clinical correlation with anti‐peripheral‐nerve myelin antibodies in Guillain‐Barré syndrome
Author(s) -
Koski Carol L.,
Gratz Edward,
Sutherland John,
Mayer Richard F.
Publication year - 1986
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410190609
Subject(s) - guillain barre syndrome , antibody , medicine , titer , myelin , complement fixation test , pathophysiology , antibody titer , peripheral , immunology , peripheral nervous system , antigen , pathology , central nervous system , serology
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.