4.0 Article

Elevated plasma factor VIII and von Willebrand factor in women with type 2 diabetes: inflammatory reaction, endothelial perturbation or else?

期刊

BLOOD COAGULATION & FIBRINOLYSIS
卷 22, 期 7, 页码 600-605

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MBC.0b013e32834b2fe1

关键词

endothelial dysfunction; factor VIII; inflammation; type 2 diabetes; von Willebrand factor

资金

  1. Fundacao de Amparo a Pesquisa de Minas Gerais (FAPEMIG)
  2. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)

向作者/读者索取更多资源

The association between type 2 diabetes and cardiovascular disease is long recognized. Although perturbations of haemostatic markers have been shown to be associated with macrovascular disease in patients with type 2 diabetes, it is unclear whether these are primarily due to endothelial dysfunction or a result of inflammation. The present study was undertaken to elucidate whether elevated levels of factor VIII (FVIII) and von Willebrand factor (vWF) in women with type 2 diabetes represent endothelial dysfunction, inflammation or an alternate mechanism. Sixty-four women with type 2 diabetes were evaluated using ultrasonography Doppler for carotid intima-media thickness (IMT) and were classified as group A - having no (<1 mm), group B-mild (>= 1 mm and no plaque) and group C - moderate (>= 1 mm and presence of plaque and stenosis) macrovascular disease. Several haemostatic markers including, FVIII, vWF and fibrinogen were assessed. In addition, thrombomodulin, a marker for endothelial damage, and high-sensitivity C-reactive protein (hsCRP), an inflammatory marker, were also measured. A significant association of elevated FVIII was found in group B and C patients (i.e. patients with IMT >= 1 mm and with plaque). Elevated fibrinogen and vWF levels were also found but confined to group C patients. No significant difference amongsubgroups was found for any other variable evaluated (hsCRP, thrombomodulin and FVII). In conclusion, plasma FVIII levels are elevated in women with type 2 diabetes and macrovascular disease. It also appears that this is not mediated by inflammation or endothelial injury and is likely to be due to an alternate mechanism. Blood Coagul Fibrinolysis 22:600-605 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.0
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据