title: Anti-GT1a IgG in Guillain-Barré syndrome.
abstract: OBJECTIVE
  To investigate the presence of serum anti-GT1a IgG in Guillain-Barré syndrome (GBS) and its relation to clinical manifestations.
  
  
  BACKGROUND
  Several patients with GBS and bulbar palsy have been reported to have serum anti-GT1a IgG. Most, however, also have anti-GQ1b IgG. A previous study failed to detect GT1a in human cranial nerves, but GQ1b was abundant in human ocular motor nerves. Whether anti-GT1a IgG itself determines the clinical manifestations is not yet clear.
  
  
  METHODS
  The association of clinical manifestations with the presence of anti-GT1a IgG and with its cross reactivity was investigated. An immunochemical study was performed to determine whether GT1a is present in human cranial nerves.
  
  
  RESULTS
  Anti-GT1a and anti-GQ1b IgG were positive in 10% and 9% respectively of 220 consecutive patients with GBS. Patients with anti-GT1a IgG often had cranial nerve palsy (ophthalmoparesis, 57%; facial palsy, 57%; bulbar palsy, 70%), and 39% needed artificial ventilation. These features were also seen in patients with anti-GQ1b IgG. There was no significant difference between the two groups with respect to the frequency of clinical findings. An enzyme-linked immunosorbent assay showed that anti-GT1a IgG cross reacted with GQ1b in 75% of the patients, GD1a in 30%, GM1 in 20%, and GD1b in 20%. All five patients who carried anti-GT1a IgG that did not cross react with GQ1b had bulbar palsy, neck weakness, absence of sensory disturbance, and positive Campylobacter jejuni serology. Thin-layer chromatography with immunostaining showed that GT1a is present in human oculomotor and lower cranial nerves.
  
  
  CONCLUSIONS
  These findings provide further evidence that anti-GT1a IgG itself can determine clinical manifestations. The distinctive clinical features of patients with anti-GT1a IgG without anti-GQ1b activity distinguish a specific subgroup within GBS.
authors.affiliation: Department of Neurology and Clinical Neuroscience Yamaguchi University School of Medicine, Yamaguchi, Japan. kogamrk@dokkyomed.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Koga
authors.forename: H
authors.initials: H
authors.lastname: Yoshino
authors.forename: M
authors.initials: M
authors.lastname: Morimatsu
authors.forename: N
authors.initials: N
authors.lastname: Yuki
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000032:analysis*; D002855:Chromatography, Thin Layer; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D020275:Guillain-Barre Syndrome / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis / Q000276:immunology*; D008297:Male; D008875:Middle Aged
chemical_list: D001323:Autoantibodies; D007074:Immunoglobulin G