The Percentage of Neutrophils is Independently Associated with Blood-Brain Barrier(BBB) Disruption in Myelin Oligodendrocyte Glycoprotein Antibody Associated Disease (MOGAD)

中性粒细胞百分比与髓鞘少突胶质细胞糖蛋白抗体相关疾病 (MOGAD) 中的血脑屏障 (BBB) 破坏独立相关

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Abstract

PURPOSE: This study aims to investigate the risk factors associated with blood-brain barrier(BBB) disruption in patients with myelin oligodendrocyte glycoprotein antibody associated disease(MOGAD). PATIENTS AND METHODS: We collected clinical data from 95 patients diagnosed with MOGAD at the Department of Neurology, the First Affiliated Hospital of Zhengzhou University from October 2018 to May 2024. Patients were classified into normal or damaged BBB groups based on cerebrospinal fluid (CSF) albumin/serum albumin (QAlb). Binary logistic regression analysis was used to evaluate the risk factors for BBB disruption in MOGAD patients. RESULTS: Our study revealed that in MOGAD patients with BBB damaged, there is a higher proportion of acute phase high EDSS scores, higher incidence of prodromal symptoms, and a higher rate of viral infections. Myelitis is the main clinical phenotype, with clinical manifestations primarily including limb weakness and bladder/bowel dysfunction. Laboratory tests showed higher levels of CSF protein, immunoglobulin (IgG), 24-hour intrathecal IgG synthesis rate, peripheral blood leukocytes, neutrophil percentage, NLR, anti-thyroglobulin antibodies(TGAbs), and fibrinogen levels, while free triiodothyronine (FT3) and lymphocyte percentage were lower. Multivariate regression analysis indicated that an increased neutrophil percentage is an independent risk factor for BBB damage in MOGAD patients (OR=1.068, 95% CI: 1.018-1.122, P=0.008). CONCLUSION: Neutrophil percentage is a readily available and widely used indicator reflecting the immune system's state and the body's inflammation level. The change in neutrophil percentage is independently associated with BBB damage in MOGAD patients. This finding helps provide more reference information for personalized treatment decisions and further research into the pathogenesis of MOGAD.

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