الفهرس 
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Abstract
-95- Summary and Conclusion
SUMMARY AND CONCLUSION
Pre-eclampsia is a pregnancy specific disorder complicating 5% to 7% of pregnancies, and characterized by hyper-tension, proteinuria, oedema and activation of the heaemostatic system. Pre-eclampsia is one of the major causes of maternal and prenatal morbidity and mortality (Sibai et al, 1994).
The pathogenesis of pre-eclampsia remains obscure, insufficient placentation has been implicated as the underlying cause of the disease (Redman, 1991). In the development of maternal manifestations of pre-eclampsia, dysfunction of the vascular endothelial cells is considered to play a major role (Roberts et al, 1989).
It is known that there is insulin resistance in normal pregnancy (Catalano et al, 1991). As well as an association between the degree of insulin elevation and hypertension during the third trimester (Bauman et al, 1982). It has been suggested that insulin resistance might be common aetiologic factor causing hyperinsulinaemia, hypertension hyper triglyceridaemia and low serum LDL-C, a cluster of risk factors for coronary artery disease also designated
-96- Summary and Conclusion
”syndromeX” (Reaven, 1988) or insulin resistance syndrome (Ferannini et al, 1991).
Lorentzen et al, (1994) hypothesized that alterations in circulating lipids may contribute to the induction of endothelial dysfunction in patients with pre-eclampsia.
Both TXA2 and PGI2 production arc increased during pregnancy, but the increase in PGI2 far exceeds the increase in TXA2 (Fitzgerald et al, 1987).
The reduction in PGI2 precedes the clinical development of pre-eclampsia, and increase in TXA2 biosynthesis can be detected (Fitzgerald et al, 1990, Van Asche et al, 1993).
The aim of this work is to investigate the serum levels of insulin and TXA2, and their roles in pathogenesis of pregnancy induced Hypertension.
The study included 40 patients with pregnancy induced hypertension and 40 normotensive pregnant women, as control, in the third trimester of pregnancy. They were subjected to complete history taking, general, obstetrical examination measuring of serum levels of insulin and thromboxane A2 urinary metabolite via radioimmuno assay. The results were compared statistically.
-97- Summary and Conclusion
Results (1) The pre-eclamptic women showed statistically significant elevation of mean serum insulin and urinary TXA2 metabolites compared with normally healthy pregnant women (Table 2, Table 3).
(2) Mean Serum insulin levels showed no statistically significant cnanges between different age group and gestational age groups in both control and study cases. Also no significant changes were detected when different age and gestational age groups of Control and study cases are compared.
In the present work, no statistically significant change is detected between different age groups or between different gestational age groups of pre-eclamptic women (P < 0.05) (Table 4). Several studies reported an increase in TXB2 and a decrease in PGI2 metabolites in venous blood of preeclamptic women.
Preeclamptic patients showed significant rise in TXB2 in the third trimester, while the concentration falls in their normotensive counterparts (Greer et al, 1985).
However kaaja et al (1995) reported that urinary metabolites of TXA2 showed no change in hypertensive pregnant women.
-98- Summary and Conclusion
This imbalance can be a sequence of endothelial cell injury altering the PGI2/TXA2 relationship with a subsequent activation of platelets and microangiopathy.
The imbalance between TXA2 and PG’, is further associated with increased levels of lipid peroxides and compounds which can damage endothelial cells and inhibit PGI2 production (Wang et al, 1992).
It has been suggested that insulin might be a common aetiologic factor causing hyperinsulinaemia, hypertension hypertriglyceridaemia and low serum HDL. (Ferannini et al, 1991).
Insulin resistance in adipocytes causes lipolysis with enhanced flux of free fatty acids to the liver.
Further more the increased hepatic uptake of free fatty acids may itself reduce portal insulin excretion by the liver resulting in higher peripheral insulin levels (Jensen et al, 1989).
Endothelial dysfunction is therefore experience Of pre-eclampia both directly and indirectly through the generation of small dense LDL. Small denses LDL is more susceptible to oxidation. Oxidized LDL inhibits endothelial PGI2 synthesis,
-99- Summary and Conclusion
inactivates endothelium derived relaxing factor (4, 14) & simultaneously increase endothelin production and release.
These changes promote platelet activation with resultant enhanced TXA2 release.
-100- .S’unitnary and Conclusion
CONL USION
•Pre-eclamptic pregnant women exhibit hyper insulinaemia and statistically significant elevation of urinary metabolites of TXA2, Compared to normally pregnant women.
•No consistent conclusions could be obtained regarding the changes of insulin and urinary metabolites of TXA2 with age and gestational age.
•In pre-eclamptic women, enhanced TXA2 release may follow hyperinsulinaemia with abnormal lipid profile causing impaired release of PGI2 and platelet activation.
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