Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 16

Abstract

Antibodies to different neural antigens have been reported in patients with dysimmune neuropathies but their pathogenetic role in these diseases is still debated. In order to identify other possible protein target antigens in these diseases we tested by immunoblot IgG and IgM reactivity with human cauda equina and spinal cord in the sera from 30 patients with Guillain‐Barré syndrome (GBS), 14 with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and 11 with multifocal motor neuropathy (MMN). As controls we examined sera from 11 patients with amyotrophic lateral sclerosis (ALS), 68 with other neurological and non‐neurological diseases (OND) and 28 normal subjects. We found high titers (>1/800) of IgG antibodies to some protein bands of the approximate molecular weight (MW) of 45–50 kDa in spinal cord but not cauda equina, in 20 patients (67%) with GBS, and 1 each with MMN and CIDP (9% and 7%, respectively)(GBS vs. MMN/CIDP p < 0.05). In 16 GBS positive patients this reactivity was re‐tested and found reduced during recovery. A similar IgG reactivity with the 45–50 kDa bands was found in 2 patients (18%) with ALS (GBS vs. ALS p < 0.05), 15 (23%) with OND (GBS vs. OND p < 0.001) and in no normal subject. Since the MW of reactive bands corresponded to that of Glial Fibrillar Acidic Protein (GFAP), we tested the serum from 6 intensely positive GBS patients (titers of 1/6400 up to 1/12800) for IgG reactivity with purified GFAP by immunoblot. In four of them IgG bound to GFAP in a pattern similar to that observed with a commercial anti‐GFAP antibody. Pre‐incubation of one of these sera with purified GFAP completely abolished IgG reactivity with GFAP by immunoblot. This study shows that anti‐GFAP IgG antibodies are significantly increased during the acute phase of GBS and decrease during recovery. Further investigation is necessary to clarify their possible pathogenetic role in the disease.