Anti-GD1a antibody is associated with axonal but not demyelinating forms of Guillain-Barre syndrome

T. W. Ho, H. J. Willison, I. Nachamkin, C. Y. Li, J. Veitch, H. Ung, G. R. Wang, R. C. Liu, D. R. Cornblath, A. K. Asbury, J. W. Griffin, G. M. McKhann

Research output: Contribution to journalArticlepeer-review

Abstract

Immunopathological studies suggest that the target of immune attack is different in the subtypes of Guillain-Barre syndrome (GBS). In acute motor axonal neuropathy (AMAIN), the attack appears directed against the axolemma and nodes of Ranvier. In acute inflammatory demyelinating polyneuropathy (AIDP), the attack appears directed against a component of the Schwann cell. However, the nature of the antigenic targets is still not clear. We prospectively studied 138 Chinese GBS patients and found that IgG anti-GD1a antibodies were closely associated with AMAN but not AIDP. With a cutoff titer of greater than 1:100, 60% of AMAN versus 4% of AIDP patients had IgG anti-GD1a antibodies; with a cutoff titer of greater than 1:1,000, 24% of AMAN patients and none of the AIDP patients had IgG anti-GD1a antibodies. In contrast, low levels of IgG anti-GM1 antibodies (> 1:100) were detected in both the AMAN and the AIDP forms (57% vs 35%, NS). High titers of IgG anti- GM1 (> 1:1,000) were more common in the AMAN form (24% vs 8%, NS). Serological evidence of recent Campylobacter infection was detected in 81% of AMAN and 50% of AIDP patients, and anti-ganglioside antibodies were common in both Campylobacter-infected and noninfected patients. Our results suggest that IgG anti-GD1a antibodies may be involved in the pathogenesis of AMAN.

Original languageEnglish (US)
Pages (from-to)168-173
Number of pages6
JournalAnnals of neurology
Volume45
Issue number2
DOIs
StatePublished - 1999

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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