Preeclampsia is a syndrome that is characterized by heterogeneous clinical and laboratory findings. The clinical features and manifestations are generally in the mother. However, sometimes the fetal syndrome may dominate the clinical picture.
The current understanding of preeclampsia has not given us an exact etiological factor or a precise pathophysiologic mechanism. However, it is becoming clear that it is much more than hypertension, proteinuria and edema in pregnancy. Despite extensive research in the pathogenesis of preeclampsia, the etiology remains a mystery. A number of mechanisms postulating the development of preeclampsia have been put forward. Some of these mechanisms have included impaired trophoblast differentiation and invasion, placental and endothelial dysfunction, immune maladaptation to paternal antigens, and exaggerated systemic inflammatory response.1 Because the disorder is heterogeneous, the pathogenesis can differ in women with various risk factors. The mechanisms underlying preeclampsia in a healthy primigravida may be quite different from those through which occur in a 40-year old chronic hypertensive woman or a woman with a previous pregnancy affected by preeclampsia.
From the public health perspective, the condition complicates 2–8% of pregnancies. Worldwide, 10– 15% of the half million maternal deaths that occur every year are associated with hypertensive disorders of pregnancy. 99% of these occur in low-resource countries. Preeclampsia also takes a massive toll on perinatal health and is responsible for a significant proportion of preterm births (iatrogenic and spontaneous), growth restriction and mortality. Preventing preeclampsia would therefore be a highly desirable goal.
