Damage to astrocytes by anti-aquaporin-4 antibody (AQP4-Ab), also known as NMO antibody, has been implicated as the cause of neuromyelitis optica. Myelin oligodendrocyte glycoprotein (MOG) is well known as the causative protein of multiple sclerosis (MS). 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. 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.
Thirty-three eyes of 23 patients with ON were studied. 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. MOG-Ab seropositivity was defined by comparing with MOG-Ab level obtained from 8 healthy normal subjects.
Eleven (47%) of 23 ON patients were NMO-Ab seropositive, while 8 (34%) of the 23 patients were MOG-Ab seropositive. Six (26%) of 23 patients were seropositive for both NMO-Ab and MOG-Ab. Ten (43%) of 23 patients were seronegative for both antibodies. 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. In the NMO-Ab(−)/MOG-Ab(−) group, visual acuity improved significantly (P < 0.0001). 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).
NMO-Ab and MOG-Ab could be potential biomarkers to determine visual prognosis in patients with ON.
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Department of Ophthalmology (TK, YU, NY, YM, RM, HG) and Division of Neurology (MM, HU), Tokyo Medical University, Tokyo, Japan; and Department of Neurology (KT), Kanazawa Medical University, Ishikawa, Japan.
Address correspondence to Takeshi Kezuka, MD, PhD, Department of Ophthalmology, Tokyo Medical University, 6-7-1 Nishi-shinjuku, Shinjuku-ku, Tokyo 160-0023, Japan; E-mail: firstname.lastname@example.org
Supported in part by a follow-up grant for the Tokyo Medical University research project and in part by a Grant-in-Aid for Scientific Research from the Japanese Ministry of Education and by the Human Health Science Foundation.
The authors report no conflicts of interest.
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