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Abstract Details

MOG Antibody Myelitis Following HIV Seroconversion
Autoimmune Neurology
P9 - Poster Session 9 (5:30 PM-6:30 PM)
9-002

A 50 year old male with asthma presented with an acute-subacute, progressive lower extremity ascending weakness, painful paresthesia that began 10 days prior to admission. On presentation his upper extremity was affected and he had impaired ability to void and defecate.  Initial exam demonstrated T3-4 sensory level with dense sensation loss in lateral three fingers, trunk, and legs, 2/5 strength in legs, hyperreflexia, and ankle clonus. MRI brain, C, T, and L spine showed T2/FLAIR signal intensity at the level of C5-C7, T1-T3 and T8-T12, with associated enhancements and enhancement in conus

CSF results showed nucleated count 79, lymphocyte 78%, glucose 51, and protein 51.  IgG index within normal limits and no oligoclonal bands were present. MOG antibody titer was 1:100.  He was treated for five days of plasma exchange and IV methylprednisolone. He was also found to be positive for HIV with CD4 count 699 and HIV viral load 4763.  From additional history, he tested negative for HIV a few months prior to obtain PrEP therapy, but did not start the medication. One month prior to symptom onset he developed flu like symptoms. Following treatment his strength improved to antigravity in lower extremities and he was discharged to rehab.

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This patient presents with probable anti-MOG antibody myelitis following the period of HIV seroconversion.  HIV has been known to cause myelitis, however this entity is exceedingly rare or underreported. This is the first case report which documents the diagnosis of probable anti-MOG antibody myelitis following period of HIV seroconversion, likely as a post-infectious sequelae of viral infection. Neuro-inflammation and demyelination are likely mechanisms, and are the proposed mechanisms of HIV associated neurologic cognitive disorders. This case could implicate the role of anti-MOG antibodies in the development of certain neurologic manifestation of HIV infection.

Authors/Disclosures
Sami Kaldawi, DO
PRESENTER
Dr. Kaldawi has nothing to disclose.
Tejas Ranade, MD (10th Medical Group) Dr. Ranade has nothing to disclose.
Zain Ashary, MD (Rush University Medical Center) Dr. Ashary has nothing to disclose.