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• W2096971678 abstract "Introduction have demonstrated an association between activation of coagulation and PAOD. Furthermore, in 1988, Boneu In addition to well-established risk factors such as showed that PAOD was associated with inhibition of fibrinolysis. In young patients (<51 years old) undersmoking, diabetes, hypercholesterolaemia and hypertension, an increasing number of novel humoral and going lower limb revascularisation, as many as 76% may have a hypercoagulable state (increased platelet endothelial factors have recently been implicated in the aetiology and progression of vascular disease. aggregation or coagulation abnormality). Thrombophilia may be defined as a propensity to thrombosis secondary to abnormalities in haemostasis. Thrombophilia has long been recognised as contributing to venous thrombosis, but is increasingly Homocysteine associated with arterial disease. It is important because screening may identify patients at high risk of thromA mild elevation of homocysteine levels (hyperbosis who may then be offered prophylaxis. This rehomocysteinaemia) affects 5% or more of the popuview will focus on the prevalence and significance of lation and is increasingly recognised as an independent thrombophilic states associated with peripheral arrisk factor for atherosclerosis and thrombosis. Hyperterial occlusive disease (PAOD) and discuss possible homocysteinaemia can cause increased Factor V acstrategies for screening and treatment. tivity, possibly via a decrease in thrombomodulin cell surface activity and a corresponding decrease in activated protein C (Fig. 1). The prevalence of hyperhomocysteinaemia in PAOD may be between 50 Prevalence of Thrombophilia and 60% and many cross-sectional studies have demonstrated a clear association between plasma General coagulation activation homocysteine levels and PAOD. If thrombophilia is important in PAOD then there should be evidence of activation of coagulation in affected patients. Thrombin and fibrinogen, and products of their metabolism, including thrombin-antiAntithrombin III thrombin (TAT) complexes, prothrombin fragments (PF) 1+2 and fibrin degradation products (FDPs) can Anti-thrombin III (AT III) is an endogenous anti-cobe used to measure coagulation activation. Crossagulant, produced by the liver, which inactivates sectional and longitudinal epidemiological studies thrombin and factor Xa. Deficiency of AT III is inherited in an autosomal dominant fashion. In a populationbased study of 7983 subjects over 55 years old 3.1% ∗ Please address all correspondence to: P. Burns, Birmingham Heartlands Hospital, Bordesley Green East, Birmingham B9 5SS. had deficiency of AT III, defined as <75% activity." @default.
• W2096971678 created "2016-06-24" @default.
• W2096971678 creator A5034701111 @default.
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• W2096971678 date "2001-08-01" @default.
• W2096971678 modified "2023-09-23" @default.
• W2096971678 title "Prevalence and Significance of Thrombophilia in Peripheral Arterial Disease" @default.
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• W2096971678 doi "https://doi.org/10.1053/ejvs.2001.1437" @default.
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