血栓调节蛋白
医学
内皮功能障碍
炎症
内皮细胞活化
血管生成素
内科学
血管生成
血管性血友病因子
内皮
脂联素
血管内皮生长因子
病理
胃肠病学
肥胖
凝血酶
胰岛素抵抗
血管内皮生长因子受体
血小板
作者
Júlia Carmona‐Maurici,Elena Cuello,David Ricart-Jané,Antonio Miñarro,Juan Antonio Baena‐Fustegueras,Julia Peinado‐Onsurbe,Eva Pardina
标识
DOI:10.1016/j.soard.2020.07.036
摘要
Background Inflammation and endothelial dysfunction are associated with morbid obesity (MO) and atherosclerosis. Objective To evaluate inflammation and endothelial function as the initial mechanisms underlying subclinical atherosclerosis in patients with MO, with and without atheromas, and their evolution after bariatric surgery (BS). Setting Arnau de Vilanova University Hospital and University of Barcelona. Methods Plasma samples from 66 patients with MO were obtained before BS and 6 and 12 months after BS. Patients were divided into 2 groups based on the presence of atheromatous plaques (detected by ultrasound imaging). Results Inflammation was increased as demonstrated by changes in the levels of fibroblast growth factor 21, adiponectin, leptin, interleukin 6, tumor growth factor α, nonesterified free fatty acids, lipoprotein(a) and C-reactive protein (CRP). Endothelial dysfunction was characterized by impaired angiogenesis (measured through angiopoietin 1 and 2 and brain-derived neurotrophic factor), vascular function (changes in endothelin 1 and thrombomodulin levels), and diapedesis (changes in intercellular and vascular cell adhesion molecules, and E- and P-selectins). Both mechanisms occurred regardless of the presence of atheromas. BS ameliorated both processes even in patients who already had subclinical atherosclerosis. However, CRP, thrombomodulin, and P-selectin levels were higher in patients with atheromas. Conclusions Endothelial dysfunction and inflammation were detected before the appearance of structural changes in vessel walls on ultrasonography images. BS might prevent or slow atherogenesis in the early stages by breaking the vicious circle between inflammation and endothelial dysfunction. CRP, thrombomodulin, and P-selectin may have a critical role in plaque development and, together with the study of endothelial dysfunction, might be useful in assessing early atherosclerosis and its evolution after BS.
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