Introduction Myelin oligodendrocyte glycoprotein (MOG) is a nervous system protein expressed by oligodendrocytes to constitute the myelin sheath. Autoantibodies against MOG have been widely described in neurological and autoimmune diseases such as MOG-IgG-associated disorder (MOGAD). Although underlying mechanisms have not yet been understood, an overlap of MOGAD and Systemic Lupus Erythematosus (SLE) has been shown in the literature. Objectives The aim of this systematic review was to assess the possible correlations between MOGAD and SLE based on reported features found in the literature that support the association of the two. Methods A keyword-based literature search was conducted, applying a ten-year filter and using the following key-words: “MOG autoantibody-associated disease and Systemic Lupus Erythematosus”; “MOG and Systemic Lupus Erythematosus” “Anti-MOG and Lupus”; “MOG and SLE”; “MOG and LUPUS” on MEDLINE/PUBMED, ScienceDirect, SciELO, LILACS and Cochrane; and “MOG antibody-associated disease and SLE” on Google Scholar. Results Eleven publications reporting on the MOGAD and SLE correlation were included in qualitative synthesis: animal experiment (1), cross-sectional (3), prospective (2), retrospective (1), non-systematic review (3), and case report (1) studies. Conclusion Not much is known about the connection between MOG-IgG-associated disorder and SLE. Unfortunately, only observational studies have been conducted in humans so far, providing us with limited data. While MOGAD features have been reported to develop in SLE patients, this is not an universal finding. In fact, many different issues impair these results, making it difficult to match the findings of different studies.
The coexistence of multiple sclerosis (MS) and central nervous system (CNS) tumors has been reported in more than 30 cases in literature. Meningiomas have been rarely seen in MS patients and their occurrence has been observed during the course of immunomodulatory drugs such as interferon beta1a and beta-1b 1-3 . We report a case of a frontal meningioma in a patient with relapsing-remitting multiple sclerosis (RRMS) treated with interferon beta-1a for seven years followed by glatiramer acetate for three years. CASE REPORTA 39-year-old Brazilian black woman had a one-month history of diplopia followed by paresthesia and weakness in the left upper limb eight months later. The patient fully recovered from both episodes, but had additional bouts of vertigo and weakness of the right hand, paraparesis with sphincter impairment and left facial paralysis in monthly intervals. Brain MRI revealed T2-weighted hyperintense lesions in periventricular, deep white matter and subcortical regions. There was no evidence of an intracranial tumor. Spinal cord MRI showed two T2-weighted hyperintense lesions in the lateral portion of C2-C3 and C7 vertebral levels with no gadolinium enhancement. Cerebrospinal fluid examination revealed 9 white blood cells/dL, 24 mg/dL of proteins and an immunoglobulin G index of 0.92. She was diagnosed as having RRMS and interferon beta-1a (22 mg three times a week) was started. After seven years, the patient' s immunomodulatory therapy was changed to glatiramer acetate due to increasing levels of serum liver enzymes. Three years later, a follow-up brain MRI showed a gadolinium-enhanced round lesion in the basal part of the left frontal lobe, with typical appearance of meningioma, in addition to characteristic demyelinating lesions as seen in MS (Figure). The patient' s expanded disability status scale score was 1.0 and her Goldmann perimetry was unrevealing. DISCUSSIONThere is some controversy in the literature about the incidence of brain tumors in MS patients 1-3 . Our patient used interferon beta-1a for seven years, when the immunomodulatory treatment was switched to glatiramer acetate. Glatiramer acetate has been found in association with breast cancer and cutaneous lymphoma, but not with a CNS neoplasm 4,5 . To the best of our knowledge, this is the first report that suggests the association of glatiramer acetate with a CNS tumor. The intracranial meningioma was asymptomatic and casually found in a routine follow-up brain MRI performed three years following the drug switch. Whether any of the immunomodulatory drugs had a role on the meningioma development or the CNS tumor occurred in this MS patient as a sheer coincidence phenomenon, remains to be clarified.
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