Molecular mimicry between gangliosides and lipopolysaccharides of Campylobacter jejuni isolated from patients with Guillain-Barre syndrome and Miller Fisher syndrome.
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Some patients developed Guillain-Barre syndrome (GBS) after being given bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. The existence of molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from a GBS patient and that between GQ1b and C. jejuni lipopolysaccharides from patients with MFS are shown herein. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies and the development of GBS and MFS. (+info)
Development of facial palsy during immunoadsorption plasmapheresis in Miller Fisher syndrome: a clinical report of two cases.
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Immunoadsorption plasmapheresis (IAP) using a tryptophan linked gel column has been shown to effectively remove serum IgG anti-GQ1b antibody which may contribute to the pathogenesis of Miller Fisher syndrome. Two patients are reported on with Miller Fisher syndrome, who developed bilateral facial palsy during IAP using a tryptophan column, while ophthalmoplegia, ataxia, and, areflexia were improving. In these patients, the titre of anti-GQ1b antibodies was reduced. The IAP using a tryptophan column has a beneficial effect on Miller Fisher syndrome but may not inhibit the development of facial palsy. The mechanism of such a dissociated effect of IAP on Miller Fisher syndrome is discussed. (+info)
Anti-GQ1b ganglioside antibody and ophthalmoplegia of undetermined cause.
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BACKGROUND/AIM: Serum antibody against ganglioside GQ1b is reported to be closely associated with immune mediated ophthalmoplegia in the Fisher and Guillain-Barre syndromes. Its presence against glycolipids, in particular ganglioside GQ1b, was investigated in patients with ophthalmoplegia of unknown origin. METHODS: 16 patients with ophthalmoplegia, the cause of which could not be confirmed from clinical findings or diagnostic testing, were tested. 34 patients who had ophthalmoplegia of definite cause, 16 healthy people, and 23 patients with typical Fisher syndrome served as the controls. The ELISA was used to check for serum antibodies against glycolipids in all study participants. RESULTS: Two of the 16 patients with ophthalmoplegia of unknown cause had serum IgG antibody against GQ1b but not against other glycolipids, and 22 of the 23 patients with typical Fisher syndrome had this antibody. No anti-GQ1b antibodies were found in the patients with ophthalmoplegia of definite cause or in the normal controls. CONCLUSION: A common underlying cause appears to bring about the pathogenesis of palsy in Fisher syndrome and in the ophthalmoplegia with positive anti-GQ1b IgG antibody, called atypical Fisher syndrome. This antibody may prove a useful clinical marker for differentiating Fisher syndrome, typical and atypical, in patients with ophthalmoplegia. (+info)