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Título

A Neuromyelitis optica case followed first-dose AstraZeneca COVID-19 vaccination

RESUMO

Case presentation: R.S, female, 64 years old, with systemic arterial hypertension, diabetes mellitus, hypothyroidism and smoker. First dose of Astrazeneca vaccine performed on 05/05/2021. On 05/23/2021, she presented with bladder retention associated with paraparesis and hypoesthesia of the lower limbs. On 05/28/2021 was hospitalized with a hypothesis of Transverse Myelitis, performed pulse therapy with Methylprednisolone 1000mg for 5 days. Data: Oligoclonal Banding (presence of identical IgG bands in CSF and serum), CSF (Cell 281 [98% lymphocytes],pt 94, glyc 59), negative anti aquaporin, non-reactive ADA, serology negative (syphilis;toxoplasmosis;varicella zoster;herpes simplex and CMV). On 07/2021 performed MRI of the brain and total spine, which showed longitudinally extensive myelitis without gadolinium enhancement, without evidence of involvement of optic nerves, CSF (normal range) and serology (without changes). Hospital discharge with neurological examination presenting no visual deficits and paraparesis and hypoesthesia with T10 level. On 10/2021 she presented with optic neuritis in the left eye which corroborates the diagnosis of Neuromyelitis optica.
Discussion: Neuromyelitis optica (NMO) and neuromyelitis optica spectrum disorders (NMOSD) are inflammatory disorders of the central nervous system characterized by severe immune-mediated demyelination associated with predominant axonal injury of the optic nerves and spinal cord (may arise in different chronologies).
Final comments: We found in the literature cases descriptions of patients who developed transverse myelitis (TM) after receiving the Oxford/AstraZeneca vaccine (contains chimpanzee adenovirus antigen as an adjuvant) and only four cases of NMO following COVID-19 vaccination (of a different type than AstraZeneca). Immunization can lead TM through different mechanisms such as a cross-reaction between foreign antigens and self-antigens, overactivation of antigen presenting cells and the subsequent autoimmune response, and polyclonal or bystander B cell activation that can lead to cytokine synthesis and activation of autoreactive T cells. In our case it could be hypothesized that the cytokine storm, leads to cell lysis and release of AQP4 molecules and might trigger humoral response in individuals with genetic susceptibility to autoimmune dis- eases. The role of adjuvants as contributing factors to the inflammatory and immune adverse vaccine reaction should be emphasized and studied.