OBJECTIVE: To investigate the presence of anti-GalNAc-GD1a antibodies in patients with Guillain-Barré syndrome (GBS) and to determine the relation of anti-ganglioside antibodies with clinical features. BACKGROUND: The GBS is heterogeneous with regard to clinical manifestations, antecedent infections, and the presence and specificity of anti-ganglioside antibodies. Recently, antibodies to minor gangliosides have been identified in serum from GBS patients. METHODS: The authors used ELISA to detect anti-ganglioside antibodies in 132 GBS patients and then correlated results with a database containing information on antecedent infections and clinical parameters. RESULTS: Anti-GalNAc-GD1a antibodies could be detected in 19 (14%) GBS patients. The presence of anti-GalNAc-GD1a antibodies was related to antecedent Campylobacter jejuni infection (p<0.001). GBS patients with anti-GalNAc-GD1a antibodies had a rapidly progressive, more severe, and predominantly distal weakness. Furthermore, they had less sensory loss, paresthesia, and cranial nerve involvement. In most patients, this reactivity was independent of reactivity to GM1. Dividing patients into separate groups based on their reactivity to GalNAc-GD1a and GM1 enabled the authors to delineate more homogeneous subgroups with regard to clinical features. CONCLUSIONS: This study provides further evidence for the hypothesis that antecedent infections and the specificity of subsequent anti-neural antibody responses determine the clinical manifestations in GBS patients.
OBJECTIVE: To investigate the presence of anti-GalNAc-GD1a antibodies in patients with Guillain-Barré syndrome (GBS) and to determine the relation of anti-ganglioside antibodies with clinical features. BACKGROUND: The GBS is heterogeneous with regard to clinical manifestations, antecedent infections, and the presence and specificity of anti-ganglioside antibodies. Recently, antibodies to minor gangliosides have been identified in serum from GBSpatients. METHODS: The authors used ELISA to detect anti-ganglioside antibodies in 132 GBSpatients and then correlated results with a database containing information on antecedent infections and clinical parameters. RESULTS: Anti-GalNAc-GD1a antibodies could be detected in 19 (14%) GBSpatients. The presence of anti-GalNAc-GD1a antibodies was related to antecedent Campylobacter jejuniinfection (p<0.001). GBSpatients with anti-GalNAc-GD1a antibodies had a rapidly progressive, more severe, and predominantly distal weakness. Furthermore, they had less sensory loss, paresthesia, and cranial nerve involvement. In most patients, this reactivity was independent of reactivity to GM1. Dividing patients into separate groups based on their reactivity to GalNAc-GD1a and GM1 enabled the authors to delineate more homogeneous subgroups with regard to clinical features. CONCLUSIONS: This study provides further evidence for the hypothesis that antecedent infections and the specificity of subsequent anti-neural antibody responses determine the clinical manifestations in GBSpatients.
Authors: J Schessl; M Koga; K Funakoshi; J Kirschner; W Muellges; A Weishaupt; R Gold; R Korinthenberg Journal: Arch Dis Child Date: 2006-08-18 Impact factor: 3.791
Authors: C W Ang; J D Laman; H J Willison; E R Wagner; H P Endtz; M A De Klerk; A P Tio-Gillen; N Van den Braak; B C Jacobs; P A Van Doorn Journal: Infect Immun Date: 2002-03 Impact factor: 3.441
Authors: Zhahirul Islam; Michel Gilbert; Quazi D Mohammad; Kevin Klaij; Jianjun Li; Wouter van Rijs; Anne P Tio-Gillen; Kaisar A Talukder; Hugh J Willison; Alex van Belkum; Hubert P Endtz; Bart C Jacobs Journal: PLoS One Date: 2012-08-27 Impact factor: 3.240