الفهرس 
Revised Hypothesis Of Blood CoagulationOnly 14 pages are availabe for public view
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Abstract
Protein Z is a vitamin K-dependent plasma protein Ca+2 -binding single chain glycoprotein. It belongs to the protease inhibitor superfamily. Its sequence is homologous to some of well known vitamin K-dependent coagulation factors such as factor VII, factor IX, factor X and protein C and protein S. In the presence of Ca+2 and phospholipids, PZ forms a complex with activated coagulation factor X and serves as a co-factor for the rapid inhibition of factor Xa by PZI, enhancing PZI activity more than 1000-fold. It is believed that normal protein Z levels are necessary for proper factor Xa inhibition. Thus, protein Z deficiency has been proposed to be associated with a procoagulant state. Many thromboembolic disorders have been reported in relation to PZ deficiency: ischemic cerebrovascular disease, coronary artery diseases, venous thromboembolic disorders, pregnancy complications , antiphospholipid syndrome and peripheral arterial disease. Unfortunatlely, however the published data concerning alteration of PZ level in these disorders were controversial and a definite pathophysiological role of PZ remains unclear. Consequently, we designed this study to clarify the role of PZ in thromboembolic disorders. In conclusion, Protein Z deficiency is a potential risk factor for arterial thrombosis. However, its role in the pathogenesis of ischemic stroke and coronary artery disease is still controversial .The same is true for PZ polymorphisms. Protein Z deficiency cotributes to pregnancy complications particularly intra uterine growth restriction and intra uterine foetal demise. Protein Z intron C G42A is significantly asssociated with recurrent pregnancy loss, however, intron F 79A allel is protective aginst this complication. Protein Z deficiency has not been proved to be an independent risk factor of deep venous thrombosis,however, R255H PZ mutation has confounding effect on the thromboembolic complication of Factor V Leiden mutation. Concomitant PZ deficiency in subjects with antiphospholipid antibody contributes to the development of the clinical features associated with antiphospholipid syndrome by unknown mechanism.So,Further studies are required to rule out the haemostatic role of PZ and the possible thrombotic consequences of its impairment. These studies must include the identification of genetic and environmental factors associated with low levels or impaired function of the PZ/ZPI system, which may help to unravel new thrombotic risk factors.