[Anti-GM1 and anti-sulphatide antibodies in systemic idiopathic vasculitis, systemic lupus erythematosus and mixed cryoglobulinaemia: Serum detection and clinical and electrophysiologic correlations]

BACKGROUND: In the last two decades increasing interest has been focused on the association between autoimmune polyneuropathies and high titers of anti-nervous serum autoantibodies. High titer of IgG anti-GM1 antibody could be detected in Guillain Barre' syndrome and in chronic painful axonal sensory immune-mediated polyneuropathy. The possible occurrence of anti-nervous autoantibodies in autoimmune diseases not limited to the nervous system is still under study. METHODS: We evaluated 29 patients with systemic lupus erythematosus (SLE), 19 with biopsy-proven renal involvement, 28 patients with mixed IgM-K/IgG polyclonal cryoglobulinaemia (18 with glomerulonephritis) and 19 with small-sized vessel ANCA-associated vasculitis (12 with renal involvement) by using a sensitive immunoenzyme method of autoantibody detection. RESULTS: Compared to controls (1/176+/-1/205; 1:204+/-1:103), we found a significant increase in plasma IgM and IgG anti-GM1 titers (1:643+/-1:531; 1:444+/-1:309) in SLE patients (p<0.0001). We also found IgM (1:3032+/-1:2844) and IgG (1:1560) anti-sulphatide titers to be higher than the control group (p<0.0001). Mean plasma IgM and IgG anti-GM1 titers of the cryoglobulinaemic patients were 1:524+/-1:403 and 1:501+/-1:415, respectively, once again higher than the controls (p<0.0001). Mean plasma IgM and IgG anti-sulphatide titers in this group were 1:1864+/-1:1189 and 1:1350 (p<0.0001). We found idiopathic systemic vasculitis patients to have significantly increased levels of anti-sulphatides IgG class autoantibodies (1:1400; p<0.0001). We found no correlation with the serologic markers for vasculitis or the clinical or histologic extent of renal involvement. Electrophysiologic studies revealed that in 38% of SLE patients (p<0.005), 61% of cryoglobulinaemic patients (p<0.01) and 42% of ANCA-related vasculitic patients (p<0.01) the abnormal titers of antineuronal antibodies were associated with clinical or subclinical evidence of neuropathy. CONCLUSIONS: In patients with systemic idiopathic or secondary vasculitis anti-GM1 and anti-sulphatide antibodies can frequently be found. Their presence should prompt an accurate neurological examination because these serologic abnormalities are significantly associated with neurologic, often subclinical, involvement. Antineuronal reactivity might be the epiphenomenon of primary phylogistic damage, which exposes normally segregated neuronal epitopes or be directly involved in triggering neurological injury.