الفهرس 
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Abstract
Summary and Conclusion
131 Summary and Conclusion
Hypertensive disease during pregnancy, in most countries, appears to be the largest single cause of maternal death. In addtion, 20-25% of total perinatal deaths are caused by pregnancy induced hypertensive disorders. Preeclampsia complicates 6-8% of gestations exceeding 24 weeks. Parity is an important risk factor. Preeclampsia was present in 6% of nulliparas and in only 0.3% of women undergoing their second pregnancy (MacGillivray, 1983).
Increased sensitivity to various vasoactive stimuli in women with preeclampsia is well documented. Gant et aL (1973) suggested the possiblity of predicting the later development of preeclampsia by using pressor test (angiotensin infusion) early in pregnancy. Gant et aL in 1974 reported that positive roll over test correlated strongly with the results of angiotensin sensitivity test and women with a positive test have a high risk for subsequent development of hypertensive disordes in pregnancy.
Despite of the uniquity of the disease and its impact on public health, no breakthrough has yet been achieved in the understanding of its pathophysiology or in the development of a specific treatment. Many theories and researches have been devoted to etiology of preeclampsia but over the past decade substantial evidences have demonstrated a role for prostaglandins in preeclampsia. Current knowledge implicates an imbalance between thromboxane and prostacyclin and this appears to play
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a pivotal role in the clinical and heamatological manifestations of hypertensive disorders.
Although the therapeutic effects of aspirin had been appreciated for nearly a century, it was not until 1921 that Vane described elaborate experiments in guinea pig lung which suggested that aspirin inhibits synthesis of prostaglandins. Low doses of aspirin preferentially inhibit platelet thromboxane synthesis leaving endothelial prostacyclin synthesis relatively intact. Low dose aspirin intake during pregnancy has no effect on teratogenicity, maternal or fetal bleeding complications, prolongation of gestation and increase perinatal mortality. The benefits of restoring the balance between prostacyclin to thromboxane have become obvious after several reports over the past decade which suggested that preeclampsia was associated with excessive thromboxane production compared with prostacyclin. So, the present study was addressed to evaluate the effect of low dose aspirin intake daily on thromboxane and prostacyclin production in pregnancy and also on the incidence of occurrence of hypertensive disorders and its effect on fetal weight.
In this study, sixty primigravidae with positive roll over test were divided randomly into two equal groups. The first group received low dose aspirin daily (75 mg) starting from the 28th. weeks gestation while the second group received tonics only.
Routine antenatal care was done for all pregnant women with blood samples drawn at 28, 32, 36 weeks gestation and at delivery to determine
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the plasma levels of thromboxane and prostacyclin and the thromboxane prostacyclin ratio. After delivery, the fetal weights of all pregnant women were recorded and clinical examination of fetuses was done. Statistical analysis of the results revealead the following data:
In non aspirin users, the plasma thromboxane mean values decreased from 28 to 32 weeks followed by a steady increase. At delivery, its level is higher than 28 weeks. In patients who developed PIH, such increase is significantly much higher than normotensives.
With low dose aspirin intake, plasma thromboxane mean values are significantly decreased till 32 weeks then increased till delivery time. However, the net level at delivery time is similar to that observed at 28 weeks. In patients who developed PIH, plasma thromboxane mean value shows significant increase at delivery time compared to 28 weeks level.
In non aspirin users, the plasma prostacyclin mean values are steadily increased from 32 weeks till delivery. However, in patients who developed PIH, plasma prostacyclin mean values are steadily decreased as pregnancy advances.
With low dose aspirin, intake plasma prostacyclin mean values are steadily increased till delivery lime. However, in patients who developed PIH, there is non significant change in plasma
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prostacyclin levels at the diffierent studied gestational intervals. Meanwhile, low dose aspirin signficantly increases prostacyclin levels compared to non aspirin users.
In non aspirin users, the thromboxane / prostacyclin ratio decreases from 28 to 32 weeks followed by a steady level at 36 weeks then increases at delivery. The ratio at delivery is higher than at 28 weeks. In patients who developed PIH the ratio is steadily increased starting from 32 weeks till delivery time. This increase is caused by the increase of plasma thromboxane levels.
With low dose aspirin intake, thromboxane / prostacyclin ratio is significantly decreased at delivery time compared to 28 weeks. In patients who developed PIH, the ratio is significantly increased at delivery time compared to 28 weeks. There is a significant decrease in the ratio in aspirin users compared to non aspirin users starting from 32 weeks.
-Low dose aspirin intake decreases significantly the incidence of preeelampsia while it has no effect on development of PIH.
-Low dose aspirin intake significantly improves the fetal weight with no effect on gestational length.
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Conclusion:
from the present study, we may conclude:
▪Pathophysiology of development of PIH is highly related
to increase of the plasma thromboxane levels (a potent vasoconstrictor) with concomitent decrease of plasma prostacyclin levels (a potent vasodilator) resulting in increase of the thromboxane / prostacyclin ratio.
Low dose aspirin intake (75 mg daily ) reduces the thromboxane levels with insignificant effect on prostacyclin and hence decreases the thromboxane / prostacycl in ratio.
-As a function of the drug, low dose aspirin reduces the
incidence of development of preeclampsia in high risk group.
-As a result of decreased the vasoconstrictor thromboxane,
placental perfusion may increase resulting in a relative significant increase in fetal weight.
▪No detectable maternal or fetal complications as a result of
low dose aspirin use were recorded in the present study.