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Ismail Fathy Ahmed EL Said
هيئة الاعداد
باحث / Ismail Fathy Ahmed EL Said
مشرف / Ayman Abdel Razek Abou Elnour
مشرف / Sherif Fekry Hendawy
مناقش / Ahmed M. Bahaa El Din Ahmed
تاريخ النشر
عدد الصفحات
145p. :
أمراض النساء والتوليد
تاريخ الإجازة
مكان الإجازة
جامعة عين شمس - كلية الطب - امراض النسا والتوليد
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Preeclampsia is one of hypertensive disorders with pregnancy which is a serious complication of human pregnancy, and is associated with significant maternal and perinatal morbidity and mortality. Preeclampsia is the second leading cause, after embolism, of maternal mortality (Fitzpatrick et al., 2009).
It occurs in about 7% to 10% of all pregnancies and results in substantial maternal and neonatal morbidity and mortality (Gulaboglu et al., 2007).
Preeclampsia can be defined as the development of hypertension, proteinuria, or both, after week 20 in a woman with previously normal blood pressure. It may be associated with many other signs and symptoms, such as edema, visual disturbances, headache, and epigastric pain (Sibai et al., 2005).
According to the criteria of the International Society of the Study of Hypertension in Pregnancy (ISSHP).Preeclampsia will be divided into mild preeclampsia and severe preeclampsia (Brown et al., 2001).
Most consider hypertension and proteinuria to be the hallmarks of preeclampsia, but the clinical manifestations of

this syndrome are very heterogeneous. Some women develop severe maternal disease requiring intensive care, whereas others remain asymptomatic with mild hypertension and proteinuria (Furuya et al., 2008).
Aims of management of preeclampsia are the following:
- Prevent convulsions
- Prevent complications, such as cerebrovascular hemorrhage, pulmonary edema, renal failure, abruptio placenta, and fetal death.
- Deliver a surviving child with minimal trauma to the mother
Magnesium sulfate is considered the standard agent for the prevention and treatment of eclamptic convulsions. The American College of Obstetricians and Gynecologists recommends the use of magnesium sulfate in every woman with a diagnosis of preeclampsia or eclampsia during labor and the postpartum period (ACOG, 2009).
There are numerous clinical trials describing the use of various methods to prevent or reduce the incidence of preeclampsia. Because the etiology of the disease is unknown, these interventions have been used in an attempt to correct theoretical abnormalities in preeclampsia. In short, randomized

trials have evaluated protein or salt restriction, calcium, zinc, magnesium, fish oil, or vitamins C and E supplementation (Beazley et al., 2005).
Traditionally, neurokinin B has been classified as neurotransmitters being found in discrete neurons and immune cells (Page, 2005).
These neuropeptides have been implicated in a variety of biological functions, such as smooth muscle contraction, vascular reactivity, pain transmission, neurogenic inflammation and the activation of the immune system (Collins et al., 2002).
Recently, this assumed dogma was challenged when the placenta, a tissue devoid of nerves, was found to be a source of neurokinin B gene expression (Page et al., 2001).
Excessive secretion of neurokinin B by the placenta could induce preeclampsia; the damaged endothelial cell in preeclampsia could also lead to reduced vasodilator and elevated vasoconstrictor (Page, 2000).
Our case-control study was conducted at Ain Shams University Hospital during the period between January 2012 and February 2013. A total of 81 pregnant women on the third trimester were included in the study, and were categorized into 3 groups:

- group I: [Control Group] (n=27): including normotensive pregnant women.
- group II: [Mild preeclampsia Group] (n=27): including women having mild preeclampsia.
- group III: [Severe preeclampsia Group] (n=27): including women having severe preeclampsia.
The median serum neurokinin B was significantly higher in women of group III [Severe preeclampsia Group] when compared to women of groups II [Mild preeclampsia Group] and I [Control Group]. The median serum neurokinin B was significantly higher in women of group II [Mild preeclampsia Group] when compared to women of group I [Control Group].
There was significant positive correlation between serum neurokinin B level and each of systolic blood pressure, diastolic blood pressure, mean arterial blood pressure, proteinuria grade by dipsticks, serum AST, ALT and creatinine. There was significant negative correlation between serum neurokinin B level and each of platelet count, gestational age at delivery and birth weight.
A plasma neurokinin-B level ≥ 72.5 ng/ml was associated with pre-eclampsia at a sensitivity of 100%, specificity of 81.5%.

A plasma neurokinin-B level ≥ 275 ng/ml was associated with severe pre-eclampsia at a sensitivity of 81.5%, specificity of 81.5%.