IMMUNOLOGICAL INVESTIGATION OF CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY

In order to investigate the hypothesis that chronic inflammatory demye linating polyradiculoneuropathy (CIDP) is an autoimmune disease relate d to the acute inflammatory form of Guillain-Barre Syndrome (GBS), we studied 40 patients, 40 age and sex matched controls with ether forms of peripheral neuropathy (ONP) and 37 controls from the same family or household (FC). We sought antibodies to gangliosides GM1 and LM1 by e nzyme linked immunoassay (ELISA) confirmed by immune-overlay. Only 6 ( 15%) CIDP patients had IgM antibodies to ganglioside GM1 (GM1) and non e had IgG antibodies. We found IgM antibodies to ganglioside LM1 in 2 (5%) and IgG antibodies in 4 (10%) CIDP patients. Antibodies of IgG or IgM class were detected by ELISA to chondroitin sulphate C or sulfati de in up to 7.5% of CIDP patients. There were IgM antibodies in 3 (7.5 %) and IgG in 4 (10%) patients against 25, 28 or 36 kD myelin proteins identified by immunoblot. Antibodies to any of these candidate myelin autoantigens were not significantly more frequent in CIDP than FC or ONP controls. Sera from 5 CIDP patients with active disease which subs equently responded to plasma exchange did not induce more demyelinatio n upon intraneural injection into rat sciatic nerve than ONP sera. Ser um turner necrosis factor alpha (TNF alpha) concentrations were not in creased in any of the CIDP patients. Serological evidence of Campyloba cter jejuni (Cj) infection was present in 4 (10%) CIDP patients. IgM a ntibodies to cytomegalovirus (CMV) were not detected in any sera. CIDP is not commonly associated with either of these infections or with an antibody-mediated response to any of these glycolipid or myelin autoa ntigens.