Serum and CSF anti-GM1 antibodies in patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy

• Published in: Journal of the neurological sciences Vol. 114; no. 1; pp. 49 - 55
• Main Authors: Simone, I.L., Annunziata, P., Maimone, D., Liguori, M., Leante, R., Livrea, P.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 1993; Elsevier Science
• Subjects: Antibodies - cerebrospinal fluid; Antibodies - immunology; Antibody; Biological and medical sciences; Chromatography, Thin Layer; Chronic Disease; Chronic inflammatory demyelinating polyneuropathy; Demyelinating Diseases - blood; Demyelinating Diseases - cerebrospinal fluid; Demyelinating Diseases - immunology; Enzyme-Linked Immunosorbent Assay; G(M1) Ganglioside - immunology; Ganglioside; GM1; Guillain-Barré syndrome; Humans; Immunoglobulin G - analysis; Immunoglobulin G - cerebrospinal fluid; Immunoglobulin M - analysis; Immunoglobulin M - cerebrospinal fluid; Medical sciences; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Neurology; Polyneuropathies - blood; Polyneuropathies - cerebrospinal fluid; Polyneuropathies - immunology; Polyradiculoneuropathy - blood; Polyradiculoneuropathy - cerebrospinal fluid; Polyradiculoneuropathy - immunology; GM1; Ganglioside; Antibody; Guillain-Barré syndrome; Chronic inflammatory demyelinating polyneuropathy; Human; Nervous system diseases; Immunological investigation; Serum; Cerebrospinal fluid; Guillain Barré syndrome; Inflammatory disease
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/0022-510X(93)90048-4

High titers of antibodies directed against gangliosides, especially GM1, are found in the serum of patients with a variety of polyneuropathies, including those of the inflammatory type. We assayed anti-GM1 IgG and IgM levels in the serum and cerebrospinal fluid (CSF) of 23 patients with Guillain-Barré syndrome (GBS) and 10 with chronic inflammatory demyelinating polyneuropathy (CIDP) to investigate whether this immune response may also be localized within the intrathecal compartment and correlate with clinical parameters such as time interval since disease onset, disability score, preceding infectious episodes, and GM1 therapy. When compared to the control group, anti-GM1 IgG was increased in the serum of 39% of GBS and 10% of CIDP patients, whereas anti-GM1 IgM was elevated in 17% of GBS and none of the CIDP patients. In both patient groups, however, anti-GM1 antibody levels were more frequently elevated in CSF than paired sera: they belonged to the IgG class in 48% of GBS and 50% of CIDP patients, and to the IgM class in 48% of GBS and 55% of CIDP patients. In the GBS group, anti-GM1 IgM serum levels inversely correlated with time elapsed between sample collection and onset of disease ( P < 0.05), whereas serum anti-GM1 IgG levels positively correlated with the loss of functional ability ( P < 0.005). Increased anti-GM1 antibodies in GBS serum were not associated with clinical or serological evidence of infectious antecedents nor with previous GM1 treatment. In both types of inflammatory polyneuropathies the origin of CSF anti-GM1 antibodies was likely peripheral rather than intrathecal, since in GBS patients anti-GM1 IgG levels in the CSF correlated with those in the serum, whereas in CIDP patients the rise in CSF anti-GM1 antibodies parallelled that of blood-brain barrier permeability. Our findings do not provide evidence that anti-GM1 antibodies play a key role in inflammatory demyelinating polyneuropathies, but suggest that the increase in anti-GM1 IgG in GBS serum may have a negative prognostic value. Further studies are necessary to clarify whether the presence of anti-GM1 antibodies in the CSF of GBS and CIDP patients may exacerbate neurological damage.