g(m2)-ganglioside and Hepatitis--Viral--Human

g(m2)-ganglioside has been researched along with Hepatitis--Viral--Human* in 2 studies

Other Studies

2 other study(ies) available for g(m2)-ganglioside and Hepatitis--Viral--Human

ArticleYear
IgM anti-GM2 antibody in a patient with Guillain-Barré syndrome subsequent to cytomegalovirus hepatitis cross reacts with N-acetylgalactosaminyl GD1a.
    Journal of neurology, neurosurgery, and psychiatry, 1998, Volume: 65, Issue:3

    Topics: Acetylgalactosamine; Adult; Autoantibodies; Cross Reactions; Cytomegalovirus Infections; G(M2) Ganglioside; Hepatitis, Viral, Human; Humans; Immunoglobulin M; Male; Polyradiculoneuropathy; Receptors, Immunologic

1998
[Guillain-Barré syndrome with high titers of anti-GM2 and anti-GalNAc-GD1a antibody following cytomegalovirus hepatitis].
    Rinsho shinkeigaku = Clinical neurology, 1997, Volume: 37, Issue:2

    A 28-year-old housewife developed motor and sensory neuropathy in both limbs with facial nerve paralysis and decreased taste sensation, two weeks after cough and sore throat with slight fever. On laboratory examination, mild increase of transaminases was found. Enzyme-linked immunosorbent assay showed that the serum had markedly high titers of IgG antibodies to GM2 (1:3,200) and Ga1NAc-GD1a (1:1,600). Serum IgM-EIA index and CF titer of cytomegalovirus were markedly high. In cerebrospinal fluid examination, protein was increased (110 mg/dl). Blink reflex indicated involvement of bilateral facial nerves. In limb motor and sensory nerves, conduction studies revealed the presence of both axonal degeneration and segmental demyelination. The diagnosis of Guillain-Barré syndrome (GBS) with facial nerve paralysis, relatively unique to CMV infection, was made. In the fourth week following the initial neurologic symptom, weakness in facial and limb muscles and sensory disturbances in both limbs were gradually improved. In about three months, conduction studies of limb nerves and CSF protein were normalized. During the clinical course above, the titers of antibodies to GM2 and Ga1NAc-GD1a, IgM-EIA index and the titer of CF of CMV were significantly decreased. Anti-GM2 antibody was reported to be found in the sera from the patient of GBS associated with CMV infection. However, there is no report of GBS patient with CMV infection whose serum showed the presence of both anti-GM2 and anti-Ga1NAc-GD1a antibodies. In this patient, antibodies to CMV, GM2 and Ga1NAc-GD1a epitopes and other unexamined or/and unknown epitopes may be related to the neuropathy. The studies of the specific antibody to react with facial nerve in the serum from GBS patients with facial nerve paralysis and the molecular mimicry between the specific ganglioside and the structure of CMV are warranted in future.

    Topics: Acetylgalactosamine; Adult; Antibodies, Viral; Autoantibodies; Biomarkers; Cytomegalovirus; Cytomegalovirus Infections; Facial Paralysis; Female; G(M1) Ganglioside; G(M2) Ganglioside; Hepatitis, Viral, Human; Humans; Immunoglobulin G; Immunoglobulin M; Polyradiculoneuropathy

1997