医学
内科学
胃肠病学
肺纤维化
发病机制
支气管扩张
纤维化
血管内皮生长因子
薄壁组织
肺
2019年冠状病毒病(COVID-19)
疾病
病理
血管内皮生长因子受体
传染病(医学专业)
作者
Nevra Güllü Arslan,Şengül Aksakal,İlker Yılmam,Selim Görgün
摘要
Although the epidemiological and clinical characteristics of COVID-19 patients have been described; the pathogenesis of the disease and its long-term consequences are still unclear. Pulmonary fibrosis is one of these late outcomes. In this study we evaluated Interleukin-17 (IL-17), vascular endothelial growth factor (VEGF), and immunoglobulin G4 (IgG4) levels of COVID-19 infected patients with different clinical course and their effect on pulmonary fibrosis in post-COVID period.In total, 90 patients were evaluated. Among the patients who presented for a control visit between 3-12 weeks after acute infection; patients with signs of pulmonary sequelae radiologically (traction bronchiectasis, interseptal thickening, disorders in parenchyma architecture) were classified as Group I (n= 32), patients who recovered without sequelae radiologically as Group II (n= 32). The Control group included healthy individuals who did not have COVID-19, and was classified as Group III (n= 26).The mean age in Group I was significantly higher than Group II and III (p<0.001). There was a statistically significant difference between the VEGF and IL-17 values based on the patient group they are in (p<0.05). Vascular endothelial growth factor values of Group I and III were significantly lower than the patients in Group II (p<0.001). IL-17 values of Group I and II were found to be significantly lower than Group III (p= 0.005). There was no statistically significant relationship between groups in terms of IgG4 values.In our study, it was observed that the profibrotic effects of VEGF, IL-17, and IgG4 were not dominant in patients who recovered with pulmonary sequelae after COVID; therefore, it is thought that different mechanisms mentioned or not yet revealed may cause this outcome.
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