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INTRODUCTION AND AIM OF THE WORK
Introduction Introduction Preeclampsia is a serious complication ofthe second halfof pregnancy that occurs with a frequency of5% to 15% . This disease is a leading cause of fetal growth retardation, infant and maternal morbidity and mortality. In the placental bed, fibrin and platelet deposition, thrombosis, and infarction occur and result in reduced placental perfusion . In severe disease disseminated intravascular coagulation may be present with platelet and fibrin deposition in many organs, including the brain, liver , and kidneys . Altered coagulability may be important in the pathogenesis ofpreeclampsia. (Robets, 1993) . Lipoprotein (a), a circulating lipoprotein particle, has been found to enhance blood coagulation by competing with plasminogen for its binding sites on fibrin clots and endothelial cells. This action is believed to be mediated by a structural homology (> 90%) between apoliopoprotcin (a) which is the carrier protein for lipoprotein (a) and plasminogen. The activation of plasminogen to form plasmin is the essential step necessary for the lysis of fibrin by plasmin (Dahlen, 1994). Many studies had demonstrated that elevated lipoprotein (a) levels are associated with atherogenesis and myocardial infarction. (Wang, et al. 1994) . Both in vitro and in vivo data indicate that lipoprotein (a) levels are elevated in preeclampsia and associated with the severity ofthe disease. This hypothesis is supported by observation of high lipoprotein (a) levels in a single family with two cases of severe preeclampsia. (Husby et al., 1996) . I
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INTRODUCTION<br />
AND<br />
AIM OF THE WORK