الفهرس 
Pre-eclampsiaOnly 14 pages are availabe for public view
 |  | from | 16 |  |  |
| | | from | 16 | | |
Abstract
Pre-eclampsia is one of the leading causes of maternal and perinatal morbidity and mortality worldwide. Nearly one tenth of all maternal deaths in Africa and Asia and one quarter in Latin America are associated with hypertensive diseases in pregnancy, a category that encompasses pre-eclampsia (Eiland et al., 2012).
Pre-eclampsia affects between 2–8% of pregnancies worldwide. Hypertensive disorders of pregnancy are one of the most common causes of death due to pregnancy. They resulted in 29, 000 deaths in 2013 – down from 37, 000 deaths in 1990 (Arulkumaran et al., 2013).
Pre-eclampsia is defined as a multi-system disease. It is mainly characterized by the new onset of hypertension and either proteinuria or end-organ dysfunction after 20 weeks of gestation in a previously normotensive woman (Sibai et al., 2003).
According to the criteria of the International Society of the Study of Hypertension in Pregnancy (ISSHP), pre-eclampsia will be divided into mild pre-eclampsia and severe pre-eclampsia (Brown et al., 2001).
Recently, severe hypertension and end-organ injury are the keystones for the severity of the disease. Proteinuria is no longer an essential criterion for diagnosis of pre-eclampsia and it was removed in 2013 by the American College of Obstetricians and Gynecologists (ACOG 2013).
Complications of pre-eclampsia can affect both the mother and the fetus. Acutely, pre-eclampsia can be complicated by eclampsia, the development of HELLP syndrome, hemorrhagic or ischemic stroke, liver damage and dysfunction, acute kidney injury, and acute respiratory distress syndrome. Fetal complications include fetal growth restriction and a potentially fetal or perinatal death (Mustafa et al., 2012).
The only known definitive treatment for pre-eclampsia is delivery of the fetus and placenta. The timing of delivery should balance the desire for optimal perinatal outcomes for the fetus while reducing maternal risks. The severity of disease and the maturity of the fetus are primary considerations. These considerations are situation-specific and management will vary with situation, location, and institution. Treatment can range from expectant management to expedited delivery of the fetus and placenta, in addition to pharmaceutical interventions. Important in management is the assessment of vulnerable maternal organ systems when possible, management of severe hypertension, and prevention and treatment of eclamptic seizures. Separate interventions directed at the fetus may also be necessary (Steegers et al., 2010).
Magnesium sulfate is considered the standard agent for the prevention and treatment of eclamptic convulsions. The ACOG recommends the use of magnesium sulfate in every women with a diagnosis of pre-eclampsia or eclampsia during labour and the postpartum period (ACOG, 2009).
Preventative measures against pre-eclampsia have been heavily studied. Because the pathogenesis of pre-eclampsia is not completely understood, prevention remains a complex issue. Supplementation with antioxidant, calcium and selenium are recommended. Also asprin intake, physical activity and smoking cessation are also recommended (WHO, 2011).
Although much research into mechanism of pre-eclampsia has taken place, its exact pathogenesis remains uncertain. Pre-eclampsia is thought to result from an abnormal placenta, the removal of which ends the disease in most cases. During normal pregnancy, the placenta undergoes process of vascularization to allow for blood flow between the mother and fetus. Abnormal development of the placenta leads to poor placental perfusion. The placenta of women with pre-eclampsia is abnormal and characterized by poor trophoblastic invasion. It is thought that this results in oxidative stress, hypoxia, and release of factors that promote endothelial dysfunction, inflammation, and other possible reactions (Mustafa et al., 2012).
Recent studies have thus suggested that extracellular HbF is involved in the pathogenesis of pre-eclampsia (Centlow et al., 2008).
Fetal hemoglobin is the main oxygen transport protein in the fetus during its last seven months. It stays in the newborn until roughly 6 months old during which it is completely replaced by adult hemoglobin. It differs from adult hemoglobin in its ability to bind oxygen with greater affinity than the adult form, giving the developing fetus better access to oxygen from the mother’s bloodstream (Lanzkron et al., 2008).
Fetal hemoglobin is a tetramer composed of four protein subunits and four heme prosthetic groups. Fetal hemoglobin is composed of two α subunits and two γ (gamma) subunits (α2γ2) as opposed to adult hemoglobin which is composed of two α (alpha) and two β (beta) subunits (Lanzkron et al., 2008).
Free hemoglobin F is a highly reactive molecule that is capable of damaging cell membranes, lipids, protein and DNA through direct oxidation and generation of reactive oxygen species. Also, it binds and inactivates nitric oxide causing vasoconstriction (Kumar et al., 2005).
Our non-interventional observational cohort study was conducted at Ain Shams University Maternity Hospital during the period between October 2014 and March 2015. A total of 120 pregnant women in the third trimester were included in the study and were categorized into 2 groups:
Group 1: [Control group] (n=60):including pregnant women at gestational age of 28 weeks to 40 weeks diagnosed with pre-eclampsia. This group was subdivided into 2 subgroups:
Group 1a:[Mild pre-eclampsia group] (n=20): including those with mild pre-eclampsia
Group 1b:[Severe pre-eclampsia group] (n=40): including those with severe pre-eclampsia
Group 2: [Control group] (n=60):including pregnant women matched for parity, age, and gestational age with no pre-eclampsia with the same inclusion and exclusion criteria
In our study, the mean maternal serum fetal hemoglobin level was significantly higher in women in the case group (pre-eclampsia group) as compared to the control group. Further more, the median serum fetal hemoglobin level in the case group was significantly higher in cases with severe pre-eclampsia when compared to cases with mild pre-eclampsia.
There was a significant positive correlation between maternal serum hemoglobin-F and systolic blood pressure and diastolic blood pressure and urinary albumin level.
On the other hand there was no significant difference between maternal serum fetal hemoglobin as regards maternal age and gestational age.
A serum hemoglobin F level ≥ 17.5 ng/ml was associated with pre-eclampsia at a sensitivity of 91% and a specificity of 96.7%.