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Plasma resistin is increased in patients with unstable angina

Plasma resistin is increased in patients with unstable angina

作     者:HU Wen-lan QIAO Shu-bin HOU Qing YUAN Jian-song 

作者机构:Department of Cardiology Cardiovascular Institute and Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100037 China 

出 版 物:《Chinese Medical Journal》 (中华医学杂志(英文版))

年 卷 期:2007年第120卷第10期

页      面:871-875页

核心收录:

学科分类:1002[医学-临床医学] 10[医学] 

基  金:This study was supported by National Social Commonweal Fund from Ministry of Science and Technology of China(No.2002DIB40092). 

主  题:resistin unstable angina inflammation atherosclerosis 

摘      要:Background Resistin, a novel adipokine linked to insulin resistance and obesity in rodents, which is derived mainly from macrophages and identified in atheromas in human, has been shown to play a potential role in atherosclerosis. Resistin levels were reported to increase in coronary artery disease (CAD), while data concerning resistin in different stages of CAD in Chinese people are lacking. The aim of this study was to assess whether plasma concentrations of resistin differed between patients with unstable and stable angina pectoris. Methods Plasma resistin levels were determined by means of enzyme-linked immunosorbent assay (ELISA) in 46 patients with unstable angina (UAP), 37 with stable angina (SAP) and 31 control subjects. Results Plasma concentrations of resistin were significantly increased in UAP group (geometric mean (interquartile range) 12.09 ng/ml (8.40, 18.08)) in comparison with SAP (9.04 ng/ml (7.09, 11.44)) and control groups (8.71 ng/ml (6.58, 11.56)). No differences in resistin levels were found between patients with SAP and controls. We also found that plasma resistin positively correlated with leukocyte counts (r=0.21, P=0.027), high sensitive C-reactive protein (hs-CRP) (r=0.25, P=0.008), and endothelin-1 (r=0.21, P=0.025) after adjustment for age, sex and BMI. Conclusion Resistin may be involved in the development of CAD by influencing systemic inflammation and endothelial activation.

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