We herein tested for autoantibodies against neurofascin (NF) 155, NF186, contactin-associated protein 1 and contactin-1 and investigated the autoantibody-related clinical features in 29 patients with CIDP from China.
Initially diagnosed as Guillain-Barré Syndrome, poor response to intravenous immunoglobulin, persistent deterioration, anti-neurofascin-155 antibodies and clinical response to steroid therapy led to diagnosis of acute-onset chronic inflammatory demyelinating polyneuropathy (CIDP).
Neurofascin antibodies were more common in patients with GBS/CIDP (14%, 8 of 59) compared to genetic neuropathy controls (3%, 3 of 111, <i>p</i> = 0.01).
Parallel fluctuation of anti-neurofascin 155 antibody levels with clinico-electrophysiological findings in patients with chronic inflammatory demyelinating polyradiculoneuropathy.
Antibodies to Contactin-1 and Neurofascin 155 (Nfasc155) have recently been associated with subsets of patients with chronic inflammatory demyelinating polyneuropathy (CIDP).
We assessed sural nerve biopsy specimens obtained from 9 patients with CIDP with anti-neurofascin-155 antibodies and 1 patient with anti-contactin-1 antibodies.
We tested autoantibodies to neurofascin-186 (NF186) and gliomedin in sera from patients with multifocal motor neuropathy (MMN, n=53) and chronic inflammatory demyelinating polyneuropathy (CIDP, n=95) by ELISA.