asialo-gm1-ganglioside and Guillain-Barre-Syndrome

Topics: Alzheimer Disease; Biomarkers; G(M1) Ganglioside; Guillain-Barre Syndrome; Hematologic Tests; Humans; Motor Neuron Disease; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Specimen Handling

To determine the epitopes of ganglioside complexes (GSCs) containing GQ1b or GT1a, we investigated their reactivity to GSCs consisting of asialo-GM1 (GA1) and GQ1b or GT1a using IgG anti-GQ1b- or anti-GT1a-positive sera. Nine anti-GQ1b-positive sera had higher activity to GA1/GQ1b than to GQ1b, only five of which reacted with GM1/GQ1b and GD1b/GQ1b. Five of 14 sera positive for GA1/GT1a and GM1/GT1a were negative for GA1/GQ1b and GM1/GQ1b. Sialic acids attached to the internal galactose of gangliotetraose can influence the reactivity of anti-GSC antibodies. Screening for antibodies to GSCs containing GA1 is useful for elucidation of the antibody-mediated pathophysiology.

Topics: Antibodies, Monoclonal; Autoantibodies; Enzyme-Linked Immunosorbent Assay; G(M1) Ganglioside; Gangliosides; Guillain-Barre Syndrome; Humans; Miller Fisher Syndrome

Antiganglioside serum antibodies from a patient treated with gangliosides were examined for cross-reactivity with lipopolysaccharides (LPSs) of Campylobacter jejuni strains associated with Guillain-Barré syndrome (GBS). The patient had no preceding infection with C. jejuni and developed chronic progressive motor polyneuropathy following parenteral ganglioside treatment. Serum IgG antibodies recognised GM1 and GD1b gangliosides as well as asialo-GM1, and cross-reactivity was observed with LPSs from C. jejuni O:2, O:4, O:19 and O:41. The results give a clear indication that gangliosides and LPSs from C. jejuni serotypes associated with GBS share common epitopes.

Topics: Adult; Antibodies; Campylobacter jejuni; Cross Reactions; Female; G(M1) Ganglioside; Gangliosides; Guillain-Barre Syndrome; Humans; Immunoglobulin G; Lipopolysaccharides; Polyneuropathies

A 68-year-old man, with Hairy Cell Leukemia developed a Guillain-Barré syndrome (G-B), 32 days after a single course of 2-Chlorodeoxyadenosine (CDA) at 0,14 mg/k/d, for five days in a two-hour-i.v. infusion and following a febrile neutropenia episode. In order to clarify whether this G-B case was related to an infection or to CDA neurotoxicity, we screened for infection-related autoimmune G-B and for antibodies (abs.) against gangliosides of peripheral nerves. Blood and urinary cultures were negative as well as serum anti-virus abs. However, serum anti-ganglioside abs. were positive for anti-asialo GM1 and anti-Gd1b. This latter finding was consistent with an autoimmune mechanism, not described until now as CDA neurotoxicity. In the present case, we do not have enough evidence to link CDA administration to the G-B syndrome. We think that it is necessary to exclude other causes of neurotoxicity before considering CDA adverse effect.

Topics: Aged; Autoantibodies; Cladribine; G(M1) Ganglioside; Gangliosides; Guillain-Barre Syndrome; Humans; Leukemia, Hairy Cell; Male