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Abstract
Pre-eclampsia (PET) is defined as new onset pregnancy related hypertension after 20 weeks of gestation with high systolic (≥140 mmHg) and diastolic blood pressures (≥90 mmHg) and proteinuria (300mg/24h) (Cunnigham et al., 2005). Preeclampsia is transient but potentially dangerous complication of pregnancy that affecting 3-5% of pregnancies (Skjaerven et al., 2002).
Although the patho-physiology of preeclampsia has not yet been fully elucidated, certain theories have been put forwards e.g. endothelial cell damage, decreased placental perfusion, changed vascular reactivity, instability between prostacyclin and thromboxane, and genetic factors (Higgins and Brennecke 1998). The basic pathology accepted currently in pre-eclampsia is the increase in the vascular sensitivity and generalized arterial constriction caused by pressor hormones responding to eicosanoids (Acromite et al, 1999).
Pre-eclampsia is a pregnancy state of hypertension associated with vascular hyperactivity and hyper-coagulation. The vascular hyperactivity of pre-eclampsia is mediated by changes in angiotensin II sensitivity and eicosanoid levels. In pre-eclampsia, not only is the angiotensin II refractoriness found in normotensive pregnancies lost, but the pressor response is also exaggerated (Sibai et al., 1990). Additionally, the imbalance between vasoactive eicosanoids seen in pre-eclampsia favors the vasoconstrictor and pro-coagulant thromboxane over the vasodilator prostacyclin .This occurs in conjunction with abnormal interactions between platelets and the vascular endothelium leading to increased platelet aggregation (Sibai,2002).
Many studies have concluded that high levels of blood androgens observed in preeclamptic patients may implicate the pathogenesis of Preeclampsia (Acromite et al, 1999 and Serine et al., 2001), Whereas, other studies have failed to show an association between the concentrations of unconjugated estrogen and androgen of the cord sera of preeclampsia patients and uncomplicated pregnancies (Troisi et al., 2003).
Androgens also have a promoting effect on the renin-angiotensin system. It also decreases PGI2 production in vitro and increase production of other eicosanoids (including thromboxane), resulting in increase in the TxA2 / PGI2 ratio that favors vascular constriction and coagulation in a way similar to that seen in pre-eclampsia. In addition, androgens can directly result in increased platelet aggregation, and when this effect is combined with the eicosanoids changes the pattern mirrors the pathophysiologic changes observed in pre-eclampsia (Acromite et al., 1999, and Bachmann et al., 1991).
Some studies have highlighted that changes in plasma progesterone in pregnant animals are the cause of preeclampsia, therefore, attentions have focused on the impact of alterations of plasma progesterone on preeclampsia in humans (Golmahammad Lou et al., 2005). In a study conducted by Belforl on isolated human artery from premenopausal nonpregnant women and from normotensive and preeclampsic pregnant women, it was established progesterone have direct in vitro activity in human omental artery from normal and hypertensive women in different hormonal states (Belforl et al., 1996).
The presented study included 40 pregnant women, who were divided into two groups: The first group included 20 normotensive pregnant women and presented as controls, in contrast to the second group, which included 20 pregnant women with documented severe pre-eclampsia.
The levels of total testosterone, free testosterone, DHEAS and progesterone, were detected in the sera of the patients and control groups by the means of enzyme-linked immunosorbant assay (ELISA). Healthy pregnant women, together with pre-eclamptic patients had been matched by age and parity, bearing in mind to unify these parameters in order to minimize the error that could be attributed to the small sample size concerning the measured parameters.
The results of the present study showed significant elevation in the maternal serum total and free testosterone levels among the pre-eclamptic cases, as compared to the normotensive pregnant women.
The hyperandrogenemia found among the pre-eclamptic group could be explained either by the documented increase in serum concentration of inhibin A in pre-eclampsia, or by deficiency in placental aromatization enzymes.
However, the absence of the significant correlation between the total and/or the free testosterone on one hand, and the mean diastolic and/or systolic blood pressures among pre-eclamptic cases on the other hand, suggests that testosterone has nothing to do with the severity of pre-eclampsia.
Regarding the mean DHEAS value, the current study showed significant negative correlation between it and the gestational age among the control group, with significant reduction in its value among the control group.
The results of the present study showed significant reduction in the maternal serum progesterone level among the pre-eclamptic cases, as compared to the normotensive pregnant women.