Plasma levels of von Willebrand factor in type 2 diabetes patients with and without cardiovascular diseases: A meta‐analysis

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Abstract

Chronic vascular complications are the major causes of death and disability of type 2 diabetes mellitus (T2DM) patients. von Willebrand factor (vWF) is involved in pathogenesis of cardiovascular diseases (CVD). Previous studies showed elevated plasma levels of vWF in T2DM patients with CVD, but the association has not been validated. The aim of this meta-analysis was to compare plasma levels of vWF in T2DM patients with and without CVD. We performed a meta-analysis based on published case-control studies of vWF in T2DM patients with and without CVD indexed in PubMed and other databases updated to April 2018. After independently assessing methodological quality and extracting data, 9 eligible studies were obtained including 576 cases and 632 controls. The standard mean difference (SMD) and 95% confidence intervals (95% CI) were calculated using random-effects model. Meta-analysis showed that plasma level of vWF was significantly higher in T2DM patients with CVD than T2DM patients without CVD (SMD = 0.61; 95% CI, 0.32-0.90; P < .00001). Subgroup and sensitivity analyses confirmed the robustness of the results. Plasma levels of vWF are significantly elevated in patients with T2DM complicated by CVD. This study helps further characterize the prognostic value of vWF for cardiovascular complications in T2DM patients.

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Most cited references 13

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Isolation and characterization of two binding proteins for advanced glycosylation end products from bovine lung which are present on the endothelial cell surface.

Martina Schmidt, Q.-J. Kao, Julian C. Esposito … (1992)

Nonenzymatic glycosylation of proteins, as occurs at an accelerated rate in diabetes, can lead to the formation of advanced glycosylation end products of proteins (AGEs), which can bind to endothelial cells, thereby altering cellular function in a manner which could contribute to the pathogenesis of diabetic angiopathy. In this report, we describe the isolation of two endothelial cell surface-associated proteins which mediate, at least in part, the interaction of AGEs with endothelium. Based on pilot studies demonstrating AGE binding activity with comparable characteristics in bovine endothelial cell and lung extracts, the material from lung was sequentially subjected to chromatography on hydroxylapatite, fast protein liquid chromatography Mono S, and gel filtration. Two distinct polypeptides, approximately 35 and approximately 80 kDa, were purified to homogeneity, each of which bound AGEs as demonstrated by competitive binding assays using cellular binding proteins immobilized on a plastic surface. NH2-terminal sequence analysis indicated that the approximately 35-kDa protein was novel, whereas the NH2-terminal sequence of the approximately 80-kDa protein was identical to that of lactoferrin. Immunocytologic studies using polyclonal antibody prepared to each of the purified polypeptides demonstrated the presence of immunoreactive material on the surface of bovine endothelial cells maintained under serum-free conditions. Furthermore, immunoelectron microscopic studies with antibodies to the approximately 35- and approximately 80-kDa AGE-binding proteins conjugated to different size colloidal gold particles confirmed the presence of the target antigens on the cell surface and suggested that they were closely associated. IgG purified from polyclonal antisera to either the 35- or 80-kDa AGE-binding proteins blocked the binding of 125I-AGE-albumin to the cell surface. These results indicate that endothelial cells express specific cell surface molecules which mediate AGE-endothelial interaction. These polypeptides represent a novel class of cell surface acceptor molecules for glucose-modified proteins which may promote degradation and/or transcytosis of the ligand, and modulation of cellular function.

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Diabetes mellitus is a major negative determinant of coronary plaque regression during statin therapy in patients with acute coronary syndrome--serial intravascular ultrasound observations from the Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome Trial (the JAPAN-ACS Trial).

Hiroyuki Daida, Tetsu Yamaguchi, Takafumi Hiro … (2010)

The Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome (JAPAN-ACS) trial has found that early aggressive statin therapy in patients with acute coronary syndrome (ACS) significantly reduces the plaque volume (PV) of non-culprit coronary lesions. The purpose of the present study was to evaluate clinical factors that have an impact on plaque regression using statin therapy. Serial intravascular ultrasound observations over 8-12 months were performed in 252 ACS patients receiving pitavastatin or atorvastatin. Linear regression analysis identified the presence of diabetes mellitus (DM) and PV at baseline as inhibiting factors, and serum remnant-like particle-cholesterol level at baseline as a significant factor significantly affecting the degree of plaque regression. Significant correlation between % change of PV and low-density lipoprotein cholesterol (LDL-C) level was found in patients with DM (n=73, P<0.05, r=0.4), whereas there was no significant correlation between the 2 parameters in patients without DM (n=178). The regression of coronary plaque induced by statin therapy after ACS was weaker in diabetic patients than their counterparts. Moreover, vigorous reduction of the LDL-C levels might induce a greater degree of plaque regression in ACS patients with DM.

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von Willebrand factor and the endothelium in vascular disease.

Andrew D. Blann (1993)

von Willebrand factor (vWF), first described in a bleeding disorder, has numerous other roles, some of which can be viewed in terms of the pathogenesis of atherosclerosis and others in the formation of thrombus. As a marker of endothelial cell injury it provides a unique opportunity to observe the events involved in conditions where vasculitis may occur, e.g. inflammatory vascular disease and diabetes. Just as low levels predispose to disease, so excessively high levels may lead to adverse cardiovascular events such as myocardial infarction and femoral artery occlusion, which may both be precipitated by thrombus. It is possible that intervention (possibly with drugs, peptides or other agents) that reduces circulating vWF, perhaps by interfering with its activity in aggregating platelets and mediating their adhesion to the sub-endothelium, or reducing its release from the endothelium, may lead to a reduction in thrombotic disease.

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Author and article information

Contributors

Ju Liu: (View ORCID Profile)

Journal

Title: Diabetes/Metabolism Research and Reviews

Abbreviated Title: Diabetes Metab Res Rev

Publisher: Wiley

ISSN (Print): 1520-7552

ISSN (Electronic): 1520-7560

Publication date Created: November 15 2019

Publication date Created: January 2020

Publication date (Electronic): July 07 2019

Publication date (Print): January 2020

Volume: 36

Issue: 1

Affiliations

[1 ]Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospitalthe First Hospital Affiliated with Shandong First Medical University Jinan China

[2 ]Graduate SchoolShandong First Medical University & Shandong Academy of Medical Sciences Jinan China

[3 ]School of MedicineShandong University Jinan China

[4 ]Department of Endocrinology, Shandong Provincial Qianfoshan Hospitalthe First Hospital Affiliated with Shandong First Medical University Jinan China