Antibody-positive Optic Neuritis Research Articles

Myelin Oligodendrocyte Glycoprotein Antibody–Positive Optic Neuritis: Clinical Characteristics, Radiologic Clues, and Outcome

To characterize the clinical phenotype of myelin oligodendrocyte glycoprotein antibody (MOG-IgG) optic neuritis. Observational case series. Setting: Multicenter. Patient/Study Population: Subjects meeting inclusion criteria: (1) history of optic neuritis; (2) seropositivity (MOG-IgG binding index > 2.5); 87 MOG-IgG-seropositive patients with optic neuritis were included (Mayo Clinic, 76; other medical centers, 11). MOG-IgG was detected using full-length MOG-transfected live HEK293 cells in a clinically validated flow cytometry assay. Clinical and radiologic characteristics and visual outcomes. Fifty-seven percent were female and median age at onset was 31 (range 2-79) years. Median number of optic neuritis attacks was 3 (range 1-8), median follow-up 2.9 years (range 0.5-24 years), and annualized relapse rate 0.8. Average visual acuity (VA) at nadir of worst attack was count fingers. Average final VA was 20/30; for 5 patients (6%) it was ≤20/200 in either eye. Optic disc edema and pain each occurred in 86% of patients. Magnetic resonance imaging showed perineural enhancement in 50% and longitudinally extensive involvement in 80%. Twenty-six patients (30%) had recurrent optic neuritis without other neurologic symptoms, 10 (12%) had single optic neuritis, 14 (16%) had chronic relapsing inflammatory optic neuropathy, and 36 (41%) had optic neuritis with other neurologic symptoms (most neuromyelitis optica spectrum disorder-like phenotype or acute disseminated encephalomyelitis). Only 1 patient was diagnosed with MS (MOG-IgG-binding index 2.8; normal range ≤ 2.5). Persistent MOG-IgG seropositivity occurred in 61 of 62 (98%). A total of 61% received long-term immunosuppressant therapy. Manifestations of MOG-IgG-positive optic neuritis are diverse. Despite recurrent attacks with severe vision loss, the majority of patients have significant recovery and retain functional vision long-term.

Diagnosis and treatment of anti-myelin oligodendrocyte glycoprotein antibody positive optic neuritis.

Anti-myelin-oligodendrocyte glycoprotein (MOG) antibody positive optic neuritis has been established as a new subset of optic neuropathy. Anti-MOG antibodies are usually measured by cell-based assay. Patients with anti-MOG antibody positive optic neuritis respond well to steroid therapy, and, while visual acuity outcomes are favorable, significant visual field defects remain. Furthermore, patients who are anti-MOG antibody positive have higher rates of recurrence compared to antibody negative patients. Based on these findings, anti-MOG antibody positive patients with optic neuritis have the characteristics of good visual outcomes, residual visual field defects, and high risk of recurrence. Tests for anti-MOG antibody are useful for the diagnosis and treatment of optic neuritis.

Successful treatment of steroid-resistant anti-aquaporin 4 antibody-positive optic neuritis with double-filtration plasmapheresis: a case report

Successful treatment of steroid-resistant anti-aquaporin 4 antibody-positive optic neuritis with double-filtration plasmapheresis: a case report

Rituximab for Frequently Recurring Anti-myelin Oligodendrocyte Glycoprotein Antibody-positive Optic Neuritis in a Child

Rituximab for Frequently Recurring Anti-myelin Oligodendrocyte Glycoprotein Antibody-positive Optic Neuritis in a Child

Diagnosis for Anti-myelin Oligodendrocyte Glycoprotein Antibody-positive Optic Neuritis

Diagnosis for Anti-myelin Oligodendrocyte Glycoprotein Antibody-positive Optic Neuritis

Clinical Characteristics of Anti-aquaporin-4 Antibody-positive Optic Neuritis

Clinical Characteristics of Anti-aquaporin-4 Antibody-positive Optic Neuritis

133 Aquaporin 4 antibody seropositivity and visual function in a UK cohort

ObjectivesTo identify clinical features of aquaporin 4 (AQP4) antibody positive optic neuritis (ON) in neuromyelitis optica (NMO) and NMO spectrum disorder (NMOSD) in a UK cohort.MethodsWe performed a retrospective review...

New-Onset Type 1 Diabetes Mellitus and Anti-Aquaporin-4 Antibody Positive Optic Neuritis Associated with Type 1 Interferon Therapy for Chronic Hepatitis C

A 60-year-old woman developed type 1 diabetes mellitus and anti-aquaporin-4 antibody positive optic neuritis during type 1 interferon therapies for chronic hepatitis C. The diabetes mellitus was elicited by interferon-α plus ribavirin therapy, while the optic neuritis was induced after interferon-β treatment, followed by interferon-α and ribavirin therapy. It is possible that type 1 interferons lead to the onset of the two autoimmune diseases by inducing disease-specific autoantibodies. Autoimmune disease is an infrequent complication of type 1 interferon treatment; however, once it has occurred, it may result in severe impairments. Patients undergoing type 1 interferon therapy should therefore be carefully monitored for any manifestations of autoimmune diseases.

Anti-Aquaporin-4 Antibody-Positive Optic Neuritis Treated with Double-Filtration Plasmapheresis

The anti-aquaporin-4 (AQP4) antibody was recently reported to be associated with neuromyelitis optica (NMO). Optic nerve involvements in many NMO cases are bilateral and the prognosis is poor. However, it has been suggested that plasma exchange is effective for those patients when steroid pulse therapy is ineffective. Herein, we report successful treatment of a patient with NMO using double-filtration plasmapheresis (DFPP). A 22-year-old woman consulted a neurologist for neck pain in March 2008. High-intensity lesions were shown in the cervical spinal cord by T2-weighted magnetic resonance imaging. On July 15, the patient was referred to our department for a headache and pain and blurred vision in the left eye. The best-corrected visual acuity was 20/50 and 20/500 in the right and left eyes, respectively, with visual field defects observed in both. After 3 courses of steroid pulse therapy, anti-AQP4 antibodies were positive. In November, the patient again noticed visual acuity loss in the left eye and was treated by additional steroid pulse therapy, which was not effective. Next, she underwent plasma exchange therapy, though it was stopped due to hypotension and dyspnea. The next day, the patient underwent DFPP treatment and visual function gradually recovered. It is important to consider NMO when steroid pulse therapy is not effective. We successfully and safely treated NMO in a young adult patient using DFPP.