Pre-eclampsia/Eclampsia in Italy Over the Years 2010-2016

Poor placentation is considered a powerful predisposing factor for pre-eclampsia. Recently, it has been suggested that the occurrence of pre-eclampsia requires a combination of an excessive or atypical maternal immune response to the trophoblast and/or exaggerated endothelial activation as well as a generalised hyper-inflammatory state resulting in endothelial dysfunction and associated increased vascular reactivity. Any factors (maternal and paternal constitutional, genetic and environmental risk factors) that enhance these responses would predispose to pre-eclampsia. The list of predisposing factors includes: extremes of maternal age, black race, previous history of pre-eclampsia, family history of pre-eclampsia, multifetal gestation, ≥ 10 years from previous pregnancy, limited sperm exposure, first paternity, pregnancies after donor insemination (assisted reproductive technology), oocyte donation or embryo donation, chronic hypertension or renal disease, rheumatic disease, maternal low birth weight, obesity and insulin resistance, pre-gestational diabetes mellitus, increased testosterone, increased homocysteine concentration, atherosclerosis (increased triglycerides and LDL, decreased HDL), maternal infections, pre-existing thrombophilia, maternal susceptibility genes and hydropic degeneration of placenta. Finally, smoking seems to be inversely correlated with pre-eclampsia. Pre-eclampsia can result in a fetal syndrome characterized by fetal growth restriction, reduced amniotic fluid, abnormal oxygenation, fetal demise and preterm birth. Moreover, women with pre-eclampsia are at increased risk for abruptio placentae, disseminated coagulopathy/HELLP syndrome, pulmonary oedema, acute renal failure, eclampsia, cerebral haemorrhage, death and cardiovascular or renal disease. Early prediction of pre-eclampsia would allow for close surveillance and preventive strategies