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• W1515079623 endingPage "203" @default.
• W1515079623 startingPage "189" @default.
• W1515079623 abstract "The Norwegian researcher Egeberg coined the term ‘thrombophilia’ in 1965, after having described for the first time the association between venous thromboembolism, occurring in the absence of any specific causes, and an inherited antithrombin III defect1. The term thrombophilia is now used to define all those inherited, acquired and/or transitory conditions that predispose to the onset of arterial or venous thromboses2,3. The crucial point regarding research into thrombophilia is the evaluation of the correct functioning of haemostasis. Haemostasis is currently defined in terms of ‘haemostatic balance’, a terminology that envelops a vast series of physiological mechanisms aimed at maintaining the blood fluid while it is in the vascular system, but preventing excessive haemorrhagic loss following endothelial damage or breaks in the wall of the blood vessel. A series of events is activated as a result of a lesion in a blood vessel. These events can be divided into successive phases according to a cascade model: the blood vessel-platelet activation phase (primary haemostasis), coagulation phase (secondary haemostasis), clot dissolution (fibrinolysis), and repair of the endothelial damage. The particular characteristics of the haemostatic process are its localisation, amplification and modulation that, in physiological conditions, are in perfect dynamic equilibrium4. These complex haemostatic functions are the result of the integrated and finely regulated action of many components, of which the main ones are the vascular endothelium, platelets, circulating and transmembrane proteins and calcium ions. The activation and amplification of the cascade and stabilisation of the coagulum are regulated by the balance between the activity of specific proteases and that of their respective allosteric and enzymatic inhibitors5. Abnormalities at any point during the coagulation cascade can cause pathological changes, characterised by haemorrhages or intravascular thromboses, depending on whether there is an insufficient or excessive response to endothelial damage6.In 1856, the Prussian pathologist Rudolf Virchow first proposed his hypothesis, which was subsequently shown to be correct and just as relevant nowadays, to explain the pathogenesis of thrombosis7. He suggested that three factors were sufficient and necessary to produce thrombosis: (i) hypercoagulability, (ii) stasis and, (iii) endothelial damage. These factors, present to variable degrees in the pathogenesis of venous thrombosis, also concur to increase the risk of thromboembolism during a normal pregnancy. Indeed, a state of hypercoagulability develops during pregnancy; this is caused by both increases of certain procoagulant factors and decreased effectiveness of inhibitory systems. Furthermore, the mechanical obstruction caused by the foetus and the vasodilatory effects mediated by the altered oestrogen/progesterone ratio result in increased blood pressure and stasis in the lower limbs. Together, these phenomena are responsible for the endothelial damage and compromise primary and secondary haemostasis.This review describes the main haemostatic changes occurring during pregnancy, focusing on aetiopathological aspects, the diagnostic procedures for evaluating the risk of thrombophilia and the appropriate diagnostic measures." @default.
• W1515079623 created "2016-06-24" @default.
• W1515079623 creator A5019108260 @default.
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• W1515079623 creator A5071075382 @default.
• W1515079623 creator A5071687195 @default.
• W1515079623 creator A5073522064 @default.
• W1515079623 date "2007-11-01" @default.
• W1515079623 modified "2023-09-23" @default.
• W1515079623 title "The cost-benefit ratio of screening pregnant women for thrombophilia." @default.
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