الفهرس 
Role of maternal anticardiolipin and anti-b2 glycoprotein i antibodies in correlation with fetal doppler in prediction of adverse pregnancy outcome in patients with preeclampsia
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Abstract
Preeclampsia is a major contributor to maternal mortality worldwide & remains a leading cause of perinatal mortality and morbidity, complicating 2–8% of pregnancies (Steegers et al., 2010)
It is characterized by an elevated blood pressure and proteinuria that develops after 20 weeks of gestation. Preeclampsia is diagnosed according to the following criteria: a blood pressure ≥ 140/90mmHg and proteinuria more than 300mg/24h or protein dipstick ≥ 1+ in ≥ 2 midstream samples 6 hours apart. Severe preeclampsia is diagnosed if systolic blood pressure increases up to 160mmHg and/or diastolic blood pressure increases up to 110mgHg, Proteinuria > 2gm/24h or protein dipstick 2+ on ≥ 2 midstream samples 6 hours apart, and the presence of symptoms or abnormal labs (NHBPEP, 2000).
The precise mechanism through which preeclampsia develops is uncertain, however an inadequate invasion of trophoblasts with consequential placental ischemia as a result of insufficiently dilated uterine spiral arteries is thought to be an initial cause in the pathogenesis of preeclampsia (Kang and Struben, 2008).
Research in the field continues to advance understanding of the underlying pathophysiology. Endothelial cell dysfunction and inflammation are considered to have a role in the pathophysiology of preeclampsia. A generalized activation of circulating leukocytes, characteristic of inflammation, has been found during preeclampsia (Redman et al., 2010)
Lee et al., (2003) demonstrated that Anti Cadiolipin Antibodies (ACA) in preeclampsia can bind to villous phospholipid with or without a cofactor and can adversely affect placental function and may suggest the possibility that ACAs may decrease placental functions in preeclampsia and cause higher incidence of IUGR. They also suggest that one cause of preeclampsia is the production of antiphospholipid antibodies which bind to the placental villous membrane antigen
The requirement of a cofactor, the anticardiolipin antibodies cofactor, anti-β2 glycoprotein I, to facilitate the binding of ACAs to phospholipids has been described recently (Raby et al., 2013)
It has been suggested that β2GPI can have a role as neutralizer of coagulation as it inhibits activation of factor X and XII and modulate ADP-dependant activation of platelets (Lutters et al., 2002).
Anti-β2 glycoprotein I antibodies can affect the trophoblast functions, react with syncytiotrophoblast and prevent intertrophoblast fusion causing inadequate trophoplastic invasion and may play a role in development of preeclampsia (Di Simone et al., 2007).
Doppler ultrasonography has become an indispensable tool in evaluating fetal well-being in pregnancies at risk for conditions such as pre-eclampsia, intra-uterine growth restriction (IUGR), and other adverse perinatal outcome. This is attributed to the fact that Doppler ultrasonography provides information on fetal and placental cardiova-scular function on the basis of the vascular resistance of the vessel being assessed. Use of umbilical artery and middle cerebral artery (MCA) Doppler has been the mainstay of assessment (Hoffman and Galan, 2009).The umbilical artery Doppler waveform provides information about placental resistance, and evaluation of MCA Doppler gives the investigator a window into the degrees of ’brain sparing’ as an indirect reflection of fetal hypoxia. A combination of the these Doppler parameters can be used today to separate the deprived from the ’normal’, but biometrically compromised, fetus to detect early hypoxia in IUGR and to precisely time delivery to avoid neurological sequale in the acidotic fetus (Galan et al., 2002).