Recurrent optic neuritis occurs in approximately 50 percent of patients, with some cases being both steroid-responsive and steroid-dependent, causing chronic inflammatory optic neuropathy (CRION). NMO-Ab and MOG-Ab could be potential biomarkers to determine visual prognosis in patients with ON. Patients with MOG optic neuritis have optic disk edema, which may be severe, bilateral, and recurrent optic neuritis. In the other 3 groups (NMO-Ab/MOG-Ab, NMO-Ab/MOG-Ab, and NMO-Ab/MOG-Ab), visual acuity did not change significantly (P = 0.53, 0.42, and 0.45, respectively). In the NMO-Ab/MOG-Ab group, visual acuity improved significantly (P < 0.0001). MOG-IgG reacts against a glycoprotein expressed on the myelin sheaths and. Three (50%) of 6 eyes of patients seropositive for both antibodies did not respond to corticosteroid pulse therapy and plasmapheresis, and visual acuity remained unchanged. Patients usually present with recurrent optic neuritis, often bilaterally with. Ten (43%) of 23 patients were seronegative for both antibodies. Six (26%) of 23 patients were seropositive for both NMO-Ab and MOG-Ab. MOG-Ab seropositivity was defined by comparing with MOG-Ab level obtained from 8 healthy normal subjects.Įleven (47%) of 23 ON patients were NMO-Ab seropositive, while 8 (34%) of the 23 patients were MOG-Ab seropositive. Patients with MOG may experience optic neuritis - inflammation of the optic nerves, in which the protective myelin sheaths are damaged, and/or transverse myelitis - inflammation of a section of the spinal cord, in which the myelin is damaged. The presence of peripapillary hemorrhages or severe optic disc edema with subretinal fluid indicates higher NO-MOG. At presentation, serum NMO-Ab was measured by immunofluorescence using HEK 293 cells transfected with AQP4-GFP, and anti-MOG1-125 antibody was measured by enzyme-linked immunosorbent assay. As one of a spectrum of opticospinal inflammatory disorders, MOG shares many characteristics with NMOSD. Thirty-three eyes of 23 patients with ON were studied. Autoantibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been reported in patients with inflammatory central nervous system disorders including. We investigated the relationship between NMO antibody (NMO-Ab) and anti-MOG antibody (MOG-Ab) and potential in patients with ON for recovery of vision. MOG antigen is currently considered as a cause of optic neuritis (ON) associated with MS because immunization with MOG antigen derived from oligodendrocytes induces murine ON with myelitis. Background: Optic neuritis (ON) is a main presenting symptom of neuromyelitis optica (NMO) and multiple sclerosis (MS). Myelin oligodendrocyte glycoprotein (MOG) is well known as the causative protein of multiple sclerosis (MS). Objective: To determine the relationship between immunological parameters (NMO-Ab, OCB, antiMOG-Ab) and clinical features and visual functions in NMO/NMOSD and MS patients with ON. Damage to astrocytes by anti-aquaporin-4 antibody (AQP4-Ab), also known as NMO antibody, has been implicated as the cause of neuromyelitis optica.
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