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العنوان
Urinary Placental Growth Factor
in Pregnancies Complicated by Intrauterine Growth Restriction
الناشر
Ain Shams University. Faculty of Medicine. Obstetrics and Gynecology Department,
المؤلف
Habib, Paules George
تاريخ النشر
2007 .
عدد الصفحات
143p.
الفهرس
Only 14 pages are availabe for public view

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Abstract

Intrauterine growth restriction (IUGR) is considered a severe complication in pregnancy (Kiely et al., 2005) and affecting up to 8% of all pregnancies and has massive short-term (increase fetal morbidity and mortality) and long-term (increase incidence of cardiovascular disease in adulthood) health implications (Wareing et al., 2005).
Traditionally, IUGR screening is based on clinical examination and identification of risk factors (Haram et al., 2006). When a small fetus is detected by ultra-sonographic examination, it is important to attempt to distinguish SGA (small for gestational age) from IUGR (intrauterine growth restriction). This can be facilitated by ultra-sonographic examination focused on the detection of markers for chromosomal abnormality, amniotic fluid volume evaluation and serial examinations monitoring fetal growth and growth symmetry as well as amniotic fluid volume changes (Baschat, 2004).
Among the various causes contributing to the development of IUGR, inappropriate placentation is a primary one. Placental development can be divided into vasculogenesis, in which an initial vascular network is formed; and angiogenesis, in which the network is remodeled. Additional blood vessels are generated by sprouting, branching and differential growth of the initial vessels to form a more mature system with larger and smaller vessels (Wallner et al., 2007).
As angiogenesis and vascular transformation are important in normal placental development, IUGR is though to result from impaired invasion of the maternal spiral arteries in early pregnancy, leading to reduced utroplacental perfusion and placental hypoxia (Kingdom, 1998).Placental hypoxia may stimulate the release of factors by the placenta which cause widespread maternal endothelial cell damage and derangement of placental angiogenesis (Kaufmann et al., 2003). What causes the deficient trophoblast invasion remains unknown. There are strong indications that angiogenic growth factors related to VEGF (vascular endothelial growth factor) may be implicated (Carmeliet et al., 2001).