Antibody detection in Guillain-Brr� syndrome

Abstract

Chromatograms with appropriate separated ganglioside fractions were overlaid with diluted patient sera, and antibody binding was detected with an alkaline phosphatase-labelled second antibody. Antiganglioside antibodies were present in the sera of 39 of 50 patients with Guillain-Barré syndrome (GBS), in 10 of 12 patients with Alzheimer's disease, and in approximately 30% of the controls. The antibodies were directed against ganglioside 3'-LM1, shown to be the major ganglioside of peripheral nerve (femoral nerve and cauda equina) in most of the positive GBS sera but also in a high proportion in the controls. No correlation was found between the severity or the course of the disease and the antibody titer. Daily parenteral administration of purified bovine brain-derived GM1 ganglioside for three months to 12 patients with Alzheimer's disease did not result in any antiganglioside GM1 antibodies. We have interpreted our findings in the following way. Human sera normally contain naturally occurring antibodies against gangliosides that in general do not cause any tissue damage. Thus, parenteral injection of gangliosides will not lead to any antibody formation.

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

“…Although case reports have suggested that IgG anti-GD1a can occur in GBS, [32][33][34][35][36] most studies have not found this association. 13,14,16,37 We suggest the association between AMAN and IgG anti-GD1a was not recognized, as most studies involved GBS populations consisting predominantly, if not exclusively, of AIDP patients.…”

Polyneuropathy attributes: a comparison between patients with anti-MAG and anti-sulfatide antibodies

“…All except one (who had predominantly motor involvement) had a sensory or sensorimotor impairment. Of the 32 patients 29 had paraproteinemia, 4 Waldenström's macroglobulinemia, 19 IgM monoclonal gammopathy of undetermined significance (MGUS), 4 IgG MGUS, 3 IgM oligoclonal gammopathy, one malignant centroblastic non-Hodgkin's lymphoma, and one MGUS with unknown M protein.…”

“…In the case of sulfatide, which is a common glycolipid in neural tissue containing a sulfate-3-galactose moiety [9,19], increased titers of serum anti-sulfatide antibodies were initially reported in patients with multiple sclerosis, idiopathic thrombocytopenic purpura, and chronic active hepatitis [17,20,23]. Recently these antibodies also have been found in sensory axonal neuropathy, in demyelinating neuropathy associated with anti-MAG antibodies and in Guillain-Barré syndrome [13].…”

Exposure to Exogenous Gangliosides and Guillain-Barré Syndrome

“…The presumed safety of gangliosides seems to be borne out by reports showing a lack of immune reactions in experimental animals [26], in healthy individuals, and among those with various illnesses who received the drug [27,28], However, there are biological find ings which suggest a pathogenic role of gan glioside exposure in G B S. First, a few rabbits inoculated with gangliosides developed pe ripheral neuropathy [29,30]. Second, al though GM 1 and the Gal(beta l-3)G alN A c epitope are widely distributed in the central and peripheral nervous system and antibodies which cross-react with Gal(betal-3)GalNAc and Gal(beta l-3)G lcN A c are common, with repeated immunizations the anti-GM l anti body response becomes more specific and re stricted in its cross-reactivities [31] and may ultimately result in autoimmune peripheral neuropathy [32], Third, reduction o f anti-G M l antibody titers by immunosuppressive agents may be followed by clinical improve ment in patients with immune-mediated mo tor neuropathies [33,34].…”