Abstract

Preeclampsia (PE) is a major cause of perinatal materno-fetal morbidity and pregnancy associated mortality. Clinically, severe PE associates maternal pregnancyinduced hypertension with signifi cant proteinuria and/ or oedema. HELLP syndrome is a form of severe preeclampsia (H = hemolysis; EL = elevated liver enzymes and LP = low platelets) and it usually develops suddenly during pregnancy (27-37 weeks of gestation). The cause of PE remains unknown, and the only known cure is delivery of the fetus and the placenta. Recent data demonstrate that a combination of genetic, epigenetic and environmental factors are involved. PE is often considered a two-stage disease. The first stage is a shallow cytotrophoblastic invasion which induces cycles of hypoxia-reoxygenation at the placental level. Subsequently, an abnormal expression pattern occurs which is  followed by the release of soluble factors and trophoblastic debris in the maternal blood flow. These stimuli trigger the second phase of the disease, the maternal syndrome. Women with a previous pregnancy complicated by PE are at an increased risk for recurrence in subsequent pregnancies. For severe preeclamptic women in an initial pregnancy, recurrence rates for any type of PE are very high, approaching 50% in some studies. Therefore, recurrent preeclampsia is clearly associated with more severe disease and with more severe associated morbidities. Futher insight into the pathophysiology of PE at the cellular and genomic levels will likely create new opportunities for prevention. Although some progress has been made in developing potential therapeutic options to prevent PE recurrence there is a great need for more reliable data to determine who will benefit most from any specific therapy.