الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 237 |  |  |
| | | from | 237 | | |
Abstract
Preeclampsia is a multisystmic disorder of unknown cause. Endothelial cell damage has recently been suggested to underlie the pathologic change in preeclamptic pregnancy. Thrombomodulin an endothelial cell surface glycoprotein act as a co-factor for thrombin catalyzed activation of protein C. activated protein C inhibits coagulation by inactivation the coagulation factor Va and VIIIa.
Pre-eclampsia (PE) is a pregnancy specific, multisystem disorder characterized by reduced organ perfusion secondary to diffuse endothelial injury.
The condition complicates about 3-6% of pregnancies worldwide. Despite extensive research, the exact etiology of pre-eclampsia remains elusive.
Severe preeclampsia is associated with increased risk of maternal mortality (0.2%) and increased rates of maternal morbidity (5%) such as convulsions, pulmonary edema, acute renal or liver failure, liver hemorrhage, disseminated intravascular coagulopathy (DIC), and stroke. These complications are commonly seen in women with preeclampsia that develops before 28 weeks (early onset PE) gestation and in those with preexisting medical conditions.
Serum uric acid levels have been reported to be significantly elevated in subjects with preeclampsia in many studies. Some authors suggest that the degree of elevation correlates with the severity of the maternal syndrome and of fetal morbidity.
Lactate Dehydrogenase (LDH) levels were significantly elevated in women with preeclampsia and eclampsia. Higher LDH levels had significant correlation with high blood pressure as well as poor maternal and perinatal outcome.
Thrombomodulin (TM); is a cell surface-expressed transmembrane glycoprotein which was originally identified on vascular endothelium. It acts as a natural anticoagulant. Endothelial injury results in TM release.
Thrombomodulin is a critical cofactor in the initiation of the protein C (PC) anticoagulant pathway. Plasma levels of thrombomodulin are regulated on a genetic basis, but more important is the dependence on a series of other atherosclerotic risk factors, such as hypertriglyceridemia, stroke, cancer, and diabetes.
In normal pregnancy, activation of platelets and release of thromboglobulin and platelet factor 4 are documented. Increased expression of thrombomodulin is now considered an independent risk factor for vascular disease.
The current study was a prospective case-control study conducted at Ain Shams University Maternity Hospital, to assess the changes in thrombomodulin level in women with preeclampsia.
In this study 123 women were included to assess the changes in thrombomodulin level, they were randomly divided into three groups: 41 patients with non sever preeclampsia, 41 normotensive pregnant women in third trimester, and 41pregnant female with sever preeclampsia, also if there is systemic affection as HELLP syndrome. Blood samples were collected before any medical intervenion and centrifuged for 20 min at 2,000 rpm. The resulting plasma samples were stored at -70°C until assayed. Plasma TM was assayed by a one-step sandwich enzyme immunoassay using monoclonal antibodies to human TM using kits. Pregnant women with history of deep vein thrombosis or known hypercoagulable state for example thrombophilia, chronic hypertension, cardiovascular, autoimmune, renal or hepatic diseases and diabetes were excluded from this study.
Regarding clinic-pathological features of pre-eclampsia patients and healthy control groups, our study found that there was high significant difference (p≤0.01) between hypertensive and normal patients regarding (hypertension, obesity and history of PET). Our study found that there was high significant difference (p≤0.01) between pre-eclampsia patients and healthy control group regarding serum thrombomodulin protein level and serum thrombomodulin protein increases significantly with mild and severe preeclampsia and HELLP syndrome and considered a good marker for evaluation of hypertensive patients with pregnancy.