Abstract

Abstract INTRODUCTION Many studies have revealed that angiogenesis and inflammation are closely linked to the pathophysiology of chronic subdural hematoma (CSDH). The development of CSDH is an inflammatory process that begins as a local inflammatory reaction of the dura meter to injury or external stimuli such as blood or CSF. This process causes neovascularization of the outer membrane of CSDH and vascular hyperpermeability. Heme oxygenase-1 (HO-1) is a key enzyme that catalyzes the degradation of heme and produces biliverdin, ferrous iron, and carbon monoxide. HO-1 expression is induced by oxidative stress, and the increasing expression seems to be protective in animal studies. We hypothesized that HO-1 has a protective impact on the severity of CSDH. METHODS This study is designed to correlate the histopathology of the outer membrane of CSDH and HO-1 level in the CSDH hematoma as an indicator of inflammatory status with the clinical presentation of patient and computed tomography (CT) radiological findings of a consecutive series of patients suffered from CSDH. This is a single-center, perspective cohort study. From 2014 to 2017, we enrolled 97 patients with CSDH, who has undergone surgical intervention (burr-hole drainage or craniotomy evacuation). We collect the clinical data, radiological information, and outer membrane and supernatant of the CSDH. We use enzyme-linked immunosorbent assay (ELISA) to measure the concentration of HO-1 in the supernatant of CSDH. RESULTS A significant negative correlation between the HO-1 and the thickness of CSDH is noted (P = .001). On increasing HO-1 by 1 ng/L, the CSDH thickness decreases by 81 mm (P < .005). CONCLUSION Our study demonstrates that HO-1, an important enzyme in angiogenesis and in the inflammation pathway, has a key impact on CSDH severity. A significant negative correlation between the HO-1 and thickness of CSDH has been proved.

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