Open AccessAntibodies to ganglioside GM1 and Campylobacter jejuni in patients with Guillain-Barre syndrome
Author(s) -
Ivana Basta,
Ljubica Šuturkova,
Ana Vujić,
S. Aleksić,
Ana Poceva,
Aleksandra Paskoska,
Katerina Milenikova,
R Trikić,
Slobodan Apostolski
Publication year - 2005
Publication title -
srpski arhiv za celokupno lekarstvo
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.135
H-Index - 17
eISSN - 2406-0895
pISSN - 0370-8179
DOI - 10.2298/sarh0504123b
Subject(s) - medicine , guillain barre syndrome , antibody , cerebrospinal fluid , immunology , acute motor axonal neuropathy , population , gastroenterology , environmental health
Guillain-Barré syndrome (GBS) is an acute immune mediated neuropathy, polyradiculoneuritis, characterized by rapid onset of symmetric extremity muscle paralysis, areflexia and albuminocytological dissociation in the cerebrospinal fluid (CSF). Recently, the heterogeneity of GBS has been noticed with definition of several GBS variants. The axonal GBS associated with anti-GM1 antibodies is the most important variant with the specific role of Campylobacterjejuni (CJ) in the induction of the disease. The role of our study was to determine the frequency of antecedent infection with CJ in the population of our patients with GBS, the association with anti-GM1 antibodies and the distribution of these antibodies within clinical forms of the disease. The diagnosis of GBS has been established in 17 patients according to clinical, electrophysiological and laboratory (CSF) criteria. The serum antibodies to 63 kDa flagellar protein isolated from CJ serotype 0:19 were determined by ELISA and Western blot and serum anti-GM1 antibodies by ELISA. In relation to the disability score two patients were ambulatory, five were ambulatory with support, seven were bedridden and two patients needed respirator. Five (29%) patients had pure motor, while 12 (71%) had sensorimotor GBS. The cranial nerves were involved in 11 (65%) and 9 (53%) patients had autonomic dysfunction. Electromyoneurography showed primary axonal, predominantly motor neuropathy in 6 (35%) and demyelinating sensorimotor neuropathy in 11 (65%) patients. The CSF protein content ranged from 0.47 to 3.88 g/L. The antecedent infection with CJ was shown by serum antibodies to CJ flagellar protein in 12 (71%) patients. Fifteen (88%) patients had IgG anti-GM1 antibodies. Twelve (71%) patients had both antibodies. In relation to the clinical form, anti-CJ antibodies were found in 8 (73%) out of 11 patients with demyelinating GBS and in 4 (66.6%) out of 6 patients with axonal GBS. The high titer of anti-GM1 antibodies was found in all patients (100%) with axonal and in 9 (82%) out of 11 patients with demyelinating GBS. The association of IgG anti-CJ and IgG anti-GM1 antibodies was found in 4 (66.6%) out of 6 patients with axonal and in 8 (73%) out of 11 patients with demyelinating GBS. The main features of our patients with GBS were high frequency of antecedent infection with CJ, unusually frequent association with anti-GM1 antibodies, and equally frequent association of anti-CJ and anti-GM1 antibodies in both, axonal and demyelinating GBS.