Maternal alpha1 Antitrypsin as a Marker of Intrauterine Growth Restriction in Pre-eclamptic Women

Intrauterine growth restriction (IUGR) is defined as a velocity of fetal growth less than the normal fetus growth potential for a specific neonate as per the race and gender. These neonates face many acute problems during peripartum and after birth .The causes of IUGR may be maternal, placental, fetal or genetic and also due to combination of any of these factors. Knowledge of etiologies of fetal growth restriction (FGR) is essential, so that future care can be targeted at prevention . It is apparent that FGR is primarily caused by placental dysfunction (PIH&PE), insufficiency that lead to reduced fetal growth overall. FGR is associated with lifelong burden of chronic diseases including metabolic, respiratory, cardiovascular and neurological deficits. Pre-eclampsia (PE) is diagnosed by the combined presentation of high blood pressure and proteinuria. New definitions also include maternal organ dysfunction, such as renal, liver, neurological or haematological complications, uteroplacental dysfunction, or FGR . In an attempt to correct fetus reduced supply the placenta release various cytokines and markers as Alpha-1 anti-trypsin (AAT). The Golgi apparatus secretes this cytokine in placental cytotrophoblast and blood vessels. AAT is antinflammatory antiprotease protective molecule. AAT rises during normal pregnancy. The suboptimal rise of AAT in pregnancy are liable for increased obstetrical complications like abortion, preterm labor. AAT levels were found decreased in placenta tissues from women with PE compared that of healthy women. Although AAT deficiency is associated with several pregnancy and placental disorders, little is known regarding AAT levels and PE .