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1.
Mol Med Rep ; 2(2): 253-7, 2009.
Article in English | MEDLINE | ID: mdl-21475821

ABSTRACT

Metabolic syndrome (MS) is closely linked to a generalized metabolic disorder referred to as insulin resistance. Disturbances in the hemostasis and fibrinolytic systems are a feature of MS. The aim of this study was to determine the concentration levels of fibrinogen and plasminogen activator inhibitor-1 (PAI-1) in a group of patients with MS with respect to a non-MS group, and to evaluate their possible relation with other risk factors in MS. The study was carried out in a total of 186 male and female non-smoking individuals aged 45-64 years, 93 with MS (ATP III criteria) and 93 without MS. Plasmatic levels of PAI-1 were measured by ELISA, and those of fibrinogen by the Claus method. The plasmatic levels of PAI-1 (men 49.2±19.8 vs. 35.0±12.2 ng/ml and women 42.0±19.7 vs. 31.6±14.6 ng/ml; p=0.0026) and fibrinogen (274.0±82.1 vs. 232.7±66.6 ng/ml; p=0.0002) were significantly higher in the MS group than in the non-MS group. PAI-1 was significantly associated with diastolic blood pressure, triglycerides and waist circumference. Fibrinogen was negatively associated with HDL-c. High plasmatic levels of PAI-1 and fibrinogen contribute to the cardiovascular risk that characterizes individuals with MS.

2.
Mol Med Rep ; 2(3): 481-5, 2009.
Article in English | MEDLINE | ID: mdl-21475854

ABSTRACT

Metabolic syndrome (MS) is associated with a high incidence rate of cardiovascular disease. It is characterized by abdominal obesity, elevated blood pressure, atherogenic dyslipidemia [high LDL-c (low density lipoprotein cholesterol) and low HDL-c (high density lipoprotein cholesterol)] and insulin resistance or glucose intolerance. In the context of MS, alterations in the plasmatic levels of some soluble forms of cell adhesion molecules can appear, e.g., soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin) and soluble CD40L (sCD40L). The objective of this study was to compare the serum levels of sVCAM-1, sE-selectin and sCD40L in MS and non-MS groups and to associate these molecules with the diagnostic criteria of MS. A total of 185 non-smokers between 45 and 64 years of age were included. Of these, 93 corresponded to the MS group and the remaining 92 to a non-MS group (according to modified ATP III criteria). The serum concentration of sVCAM-1, sE-selectin and sCD40L was determined by commercial solid phase ELISA. The results were expressed as a median and interquartile range. The MS group showed high levels of sVCAM-1 (558.9 ng/ml; 481.3-667.6 ng/ml) compared with the non-MS group (405.2 ng/ml; 361.0-470.5 ng/ml) (p<0.0001). As well, the median level of sCD40L (3.0 ng/ml; 2.1l-11.7 ng/ml) was significantly higher in the MS group than that in the non-MS group (2.6 ng/ml; 2.3-3.4 ng/ml) (p=0.0061). sE-selectin levels did not differ significantly between the groups: 73.9 ng/ml (58.3-87.0 ng/ml) and 68.5 ng/ml (51.6-97.5 ng/ml) in the MS and non-MS group, respectively. In conclusion, the serum levels of sVCAM-1 and sCD40L, but not sE-selectin, were significantly higher in patients with MS than in subjects that did not present MS. MS may therefore increase the expression of cell adhesion molecules, probably through endothelial activation.

3.
Front Biosci ; 12: 3093-103, 2007 May 01.
Article in English | MEDLINE | ID: mdl-17485284

ABSTRACT

The antiphospholipid syndrome (APS) is a disorder which is characterized by the presence of autoimmune antiphospholipid antibodies (APL) and increased risk of thrombosis and fetal loss. APL are associated with recurrent abortions in APS patients and participate in the pathogenesis of venous or arterial thrombosis, although the underlying mechanisms are poorly understood. Antigens that are targeted by APL include beta 2 glycoprotein I and prothrombin. Pathological mechanisms of APL encompass inhibition of natural anticoagulants (protein C system, tissue factor pathway inhibitor, and annexin A5), inhibition of the fibrinolytic system, activation of endothelial cells, monocytes and platelets, and complement activation. In this review, we discuss the main targets of APL and prothrombogenic mechanisms of APL.


Subject(s)
Antiphospholipid Syndrome/physiopathology , Thrombosis/physiopathology , Anticoagulants/therapeutic use , Antigen-Antibody Reactions , Antiphospholipid Syndrome/complications , Antiphospholipid Syndrome/immunology , Autoantigens/immunology , Humans , Thrombosis/complications , Thrombosis/drug therapy , Thrombosis/immunology
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