Introduction
Hypertensive disorders of pregnancy continue to be one of the leading causes of
high rates of maternal and perinatal mortality and morbidity. Hypertensive disorders
are common and form one of the deadly triad along with hemorrhage and infection
that results in much of the maternal morbidity and mortality related to pregnancy.
Worldwide, 50,000 women die each year because of pre-eclampsia. Pre-eclampsia is
defined as systolic/diastolic blood pressure values over 140/90 mm of Hg associated
with proteinuria greater than 0.3 g/l in a 24-hour urine collection or exceeding 1 g/l
in a random sample. The incidence of pre-eclampsia is commonly cited to be about
5-10% and mainly seen in late pregnancy that is at more than 30-32 weeks period
of gestation. (1) New onset non-proteinuric hypertension during pregnancy termedgestational hypertension, is followed by signs and symptoms of pre-eclampsia
almost half the time, and pre-eclampsia is identified in 3.9% of all pregnancies.(2)
Hypertension is the established risk factor for cardiovascular and renal disease, and there is a
strong association between microalbuminuria and hypertension. (3) Changes in human lifestyle,
such as delayed childbirth and diets customs, have increased the global incidence of placentalrelated disorders over the last decades. (4) Pre-eclampsia is an important cause of both maternal
and fetal morbidity and mortality in pregnant women. Therefore, identification of an effective
strategy to prevent pre-eclampsia is a priority and a challenge for research in obstetrics. (5)
nfortunately, the precise etiology of pre-eclampsia remains unknown. (5) (6) t is important that
appropriate treatment is initiated early in patients at highest risk and they are closely monitored.
There is continuing controversy over the optimal treatment of severe early onset pre-eclampsia in
pregnant patients remote from term, for whom the desire to avoid maternal organ damage is in
direct conflict with the desire to avoid neonatal complications of prematurity. Proponents of
expectant treatment of severe pre-eclampsia remote from term advocate the avoidance of poor
neonatal outcomes by delaying delivery for women with severe pre-eclampsia until serious
maternal complications are imminent or until neonatal survival can be assured reasonably.
Increasing evidence suggests that oxidative stress may play a key role in the etiology of preeclampsia. (7) (8) It is conjectured that the parameters of oxidative stress could be early markers
of endothelial dysfunction that predates clinical pre-eclampsia. Markers of oxidative stress like
serum triglycerides, free fatty acids, and malondialdehyde are increased in pre-eclampsia, are
positively correlated, and decrease within 48 hours postpartum. (9) A significant elevation of
fasting serum triglyceride level was found at 10 weeks of gestation in mild and severe preeclampsia. (10) Placental ceruloplasmin, a protein with antioxidant properties, expression is upregulated in the pre-eclampsia group vs. patients matched for gestational age. (6) Possibly,
placental hypoxia associated with pre-eclampsia increases placental ceruloplasmin expression as
has been noted for macrophages and monocytes. (11) This study aims to assess the lipid profile
and ceruloplasmin as markers for predicting the development of pre-eclampsia. The results may
give an insight into the pathophysiology of gestational hypertension and pre-eclampsia. Early
markers will further help us in screening those cases that have a high probability of developing
pre-eclampsia, which is one of the major causes of maternal and fetal mortality.
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