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Anti-aquaporin 4 antibody in Japanese multiple sclerosis: the presence of optic spinal multiple sclerosis without long spinal cord lesions and anti-aquaporin 4 antibody
Authors:Tanaka Masami  Tanaka Keiko  Komori Mika  Saida Takahiko
Affiliation:MS Centre, Utano National Hospital, Kyoto, Japan. tanaka@unh.hosp.go.jp
Abstract:

Background

Anti‐aquaporin 4 (AQP4) antibodies were found in patients with neuromyelitis optica (NMO) and Japanese optic–spinal multiple sclerosis (OSMS).

Objective

To review the clinical features and investigate anti‐AQP4 antibodies of Japanese patients with multiple sclerosis (MS), with or without long spinal cord lesions (LCL).

Methods

Anti‐AQP4 antibodies were examined in the sera of 128 consecutive Japanese patients by the immunofluorescence method using AQP4 transfected cells.

Results

The 45 LCL‐MS patients included 28 with a long spinal cord lesion extending contiguously over three vertebral segments on sagittal T2 weighted images (long T2 lesion) and 17 with segmental cord atrophy extending more than three vertebral segments. We identified 25 patients with anti‐AQP4 antibody with LCL and anti‐AQP4 antibody. Anti‐AQP4 antibody was found in 12/17 (70.6%) LCL‐MS patients with segmental cord atrophy, and in 13/28 (46.4%) LCL‐MS patients without segmental long cord atrophy (p = 0.135, Fisher''s exact test). Seropositive MS patients with LCL had more relapses than seronegative patients (p = 0.0004, Mann–Whitney U test). 9 patients with OSMS were negative for anti‐AQP4 antibody who did not show LCL.

Conclusion

These results suggest that an anti‐AQP4 antibody is found not only in MS patients with long T2 lesions but also in patients with segmental cord atrophy extending more than three vertebral segments. It is a marker of LCL‐MS showing frequent exacerbations. Japanese OSMS cases comprised those that were identical to NMO cases and those that were more closely related to classic MS.Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system. Japanese MS patients have been classified into two phenotypes: classic MS (CMS) and optic–spinal MS (OSMS).1 OSMS has been recognised since the 1950s.2 Patients with OSMS have symptoms and MRI findings in which the main lesions are confined to the optic nerve and spinal cord. In patients with OSMS, there is a higher female/male ratio; neuropathologically necrotic lesions; pleocytosis with a predominance of polymorphonuclear cells and a low frequency of oligoclonal IgG bands in CSF; a high incidence of autoantibodies in sera; long spinal cord lesions (LCL) extending more than three vertebral segments in MRI scans; and an association with a human leucocyte antigen class II allele (DPB1*0502).3Neuromyelitis optica (NMO) has been described as Devic disease, but its clinical definition has frequently been revised.4 LCL extending contiguously over three vertebral segments on sagittal T2 weighted images (long T2 lesion) is a disease marker. Current NMO criteria include unilateral optic neuritis, no restriction on onset of optic neuritis and myelitis, relapsing course and brain involvement.4,5 Recent NMO criteria stress the presence of both brain MRI abnormalities that do not meet diagnostic criteria for MS and NMO‐IgG,4 a highly specific biomarker of NMO,6 and its target antigen is the aquaporin 4 (AQP4) water channel.7The incidence of NMO‐IgG seropositivity in Japanese patients with OSMS (6/11 cases, 54%) was similar to that in NMO (33/45, 73%), and OSMS was thought to be the same disease.6 However, in that study,6 the Japanese OSMS patients had been selected using 1999 NMO criteria (Fujihara K, personal communication) that are not the same as the clinical definition of OSMS widely used in Japan.8 Their recent report showed that serum NMO‐IgG was found in 12 of 19 patients with OSMS (63%).9 We established an AQP4 antibody assay system and identified nine seropositive MS patients with LCL‐MS.10
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