Anti-GT1a IgG in Guillain-Barré syndrome. Issue 6 (1st June 2002)

• Record Type: Journal Article
• Authors: Koga, M; Yoshino, H; Morimatsu, M; Yuki, N
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 72:Issue 6(2002)
• Page Start: 767
• Page End: 771
• Publication Date: 2002-06-01
• Subjects: Guillain-Barré syndrome -- anti-GT1a IgG -- cross reactivity -- Campylobacter jejuni; GBS, Guillain-Barré syndrome -- MFS, Miller Fisher syndrome -- TLC, thin-layer chromatography -- ELISA, enzyme-linked immunosorbent assay; Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp.72.6.767
• Languages: English
• ISSNs: 0022-3050

Abstract

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.