Abstract

Campylobacter jejuni infection has been implicated in the pathogenesis of Guillain-Barré syndrome (GBS) due to production of humoral immune response against neural antigens. A case-control study was performed in a tertiary care teaching hospital for the estimation of anti-ganglioside antibodies in GBS patients and their controls. Blood samples were collected from 59 GBS cases, 58 neurological controls (NC) and 60 non-neurological control (NNC) patients for automatic estimation of IgG and IgM antibodies to seven gangliosides using EUROLineScan software. Antibodies of IgG class for GM1 were highly significant in GBS (p = 0.000) and NC (p = 0.031) compared to NNC. However GBS group was not significant (p = 0.413) compared to NC. For GM2 ganglioside, GBS and NC groups were significant (p = 0.000) compared to NNC, but GBS group was not significant (p = 0.999) compared to NC. For GM3 ganglioside, GBS and NC groups were significant (p = 0.000) compared to NNC; but GBS group was insignificant (p = 0.858) compared to NC with similar trend for all other ganglioside antibodies. When IgM class of antibodies was evaluated for GM1, GBS group was not significant (p = 0.604) whereas NC group was significant (p = 0.000) compared to NNC. GBS group was not significant compared to NC (p = 0.011). The trend was the same for GM2 antibodies. For GM3, GBS group was significant (p = 0.010) and NC was near significant (p = 0.055) compared to NNC. However GBS group was not significant (p = 0.808) compared to NC. No groups were significant (p > 0.05) in relation to the remaining gangliosides except for GQ1b where GBS group (p = 0.001) and NC group were significant (p = 0.000) compared to NNC. GBS group was also significant (p = 0.001) compared to NC and NNC. Anti-gangliosides antibodies were present in highly significant levels in the GBS group, though they were also present in the non-paralytic neurological control patients compared to the non-neurological control group.

Highlights

  • Guillain-Barré syndrome (GBS) is an acute, autoimmune serious disorder of the peripheral nerves characterized by ascending paralysis

  • Antibodies of IgG class (Figure 1) for GM1 was highly significant in GBS (p = 0.000) and neurological controls (NC) (p = 0.031) groups compared to non-neurological control (NNC) group

  • For GT1b, GBS was near significance (p = 0.051) when compared to NC group

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Summary

Introduction

Guillain-Barré syndrome (GBS) is an acute, autoimmune serious disorder of the peripheral nerves characterized by ascending paralysis. This syndrome is usually triggered by an acute infectious agent in 50% - 70% of cases after an interval of 1 to 6 weeks [1]. The implicated organisms include Campylobacter jejuni, Mycoplasma pneumoniae, hepatitis B virus, cytomegalovirus, varicella zoster virus, Epstein Barr virus, rubeola and human immunodeficiency virus. The targets of such immune attack are thought to be gangliosides present in large quantities on human nerve tissues. It is possible that wide scale immunization with any foreign antigen might evoke the same increased incidence of disease in those individuals predisposed to this complication

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