However, other clinical and laboratory findings made the diagnosis of MOGAD not straightforward. In this paper, we report three cases of ADEM, transverse myelitis and bilateral optic neuritis in people with HIV, all of whom had MOG antibodies. There is no data on the association of HIV with MOGAD, and whether clinical presentation and outcomes of MOGAD in people with HIV are similar to the general population is unclear. Globally, MOGAD is an uncommon condition, with recent reports indicating a prevalence of approximately 1.3–2.5 / 100,000, and annual incidence of approximately 3.4–4.8 / million. MOGAD is rarely associated with coexisting systemic autoimmune disorders, and infections are increasingly recognised as a significant trigger of MOGAD. Clinically, there are distinct clinical and radiological features which distinguish MOGAD from multiple sclerosis and from aquaporin-4-seropositive neuromyelitis optica spectrum disorder (AQP4 + NMOSD) that have led to MOGAD being treated as a distinct disease. Patients typically present with optic neuritis (bilateral or unilateral), transverse myelitis, acute disseminated encephalomyelitis (ADEM) and focal cortical disease. ![]() Myelin oligodendrocyte glycoprotein (MOG) auto-antibodies induce an immune-mediated demyelination with a predilection for spinal cord, optic nerves, and the brain. Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently described autoimmune inflammatory disorder of the central nervous system (CNS). The atypical clinical progression and the dilemmas in the diagnosis and treatment of these cases highlight gaps in the current knowledge of MOGAD among people with HIV that need further exploration. Our cases illustrate the diagnostic and management challenges of MOGAD in the setting of advanced HIV infection, where the risk of CNS opportunistic infections is high even without the use of immunosuppression. Her vision did not improve with immunosuppression and eventually died from sepsis. Her investigations were notable for positive MOG antibodies, positive Varicella Zoster Virus on cerebral spinal fluid (CSF) and hyperintense optic nerves on magnetic resonance imaging (MRI). The third patient, a 43-year-old mixed-race woman, presented with bilateral painless visual loss. Her rehabilitation was complicated by development of pulmonary embolism and tuberculosis. She remained paraplegic after methylprednisone and plasmapheresis treatments. The second patient, an 18-year-old black woman, presented with paraplegia and imaging revealed a longitudinally extensive transverse myelitis and had positive serum MOG antibodies. He made a significant recovery with corticosteroids but had a quick relapse and died from sepsis. The first patient, a 44-year-old black African man, presented with acute disseminated encephalomyelitis (ADEM) with positive serum MOG antibodies. We report three patients with HIV infection and myelin oligodendrocyte glycoprotein (MOG) antibodies in the setting of other central nervous system infections. There is limited data on the association between Human Immunodeficiency virus (HIV) infection and MOGAD. ![]()
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