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Hypertensive disease of pregnancy, postpartum hemorrhage and infectious syndromes in pregnancy and puerperium are the leading causes of morbidity and mortality for pregnant women around the world.1 Their frequency varies according to the country and accessibility to health care.1Hypertensive diseases, including preeclampsia, complicate 2–10% of all pregnancies.1–3 In Latin America and the Caribbean, hypertensive disorders are responsible for at least 26% of maternal deaths.3 Preeclampsia is a multifactorial disease caused by environmental factors that act over a genetic base, permitting the occurrence of this disorder.4–12 Based on this premise, the risk factors considered for the development of this disease are: overweightness; obesity; nulliparity and multiparity; being at the extremes of reproductive life; vascular diseases, such as chronic hypertension; metabolic diseases, such as diabetes mellitus; collagen diseases, such as systemic lupus erythematosus; multiple pregnancies; maternal and paternal family history12–14 (paternal imprinting expressed in the mother); pregnancy by assisted reproductive techniques;12 micropolycystic ovary syndrome with insulin resistance;15 severe anemia;16 antiphospholipid syndrome;17 and low-calcium diets consumed by people living at high altitudes.18,19 The interaction of risk factors and multiple polymorphic genes induces the synthesis of several proteins with effects differing from their original function, leading to the impairment of placental perfusion and the consequent production of mediators that damage the endothelium. The main proteins and others factors involved are listed below.7,8,20 Group I – vasoactive and vascular remodeling proteins: nitric oxide synthase; renin; type I and II angiotensin receptors; angiotensin converting enzyme; polycarboxypeptidase; endothelin-1; alpha and beta estrogen receptors; endoglin; tyrosine-kinase fms-like receptor-1; placental growth factor; and vascular endothelial growth factor.20 Group II – thrombophilia and hypofibrinolysis: methyltetrahydrofolate reductase; Leiden Factor V; prothrombin; fetal thrombophilia; plasminogen activator inhibitor-1; B3 integrin; and glycoprotein IIIA.20 Group III – oxidative stress, lipid metabolism, endothelial injury: epoxide hydrolase; glutathione transferase; superoxide dismutase; cytochrome P450 1A1; lipoprotein lipase; apolipoprotein E; and long-chain 3-hydroxyacylCoA dehydrogenase.20 Group IV – immunogenetic: human leukocyte antigen; interleukins 1 and 10; and tumor necrosis factor.20 Physiologically, in order to promote vascular remodeling, the changes of the decidua also occur in the inner area of the myometrium.21 An interaction of trophoblastic human leukocyte antigen (HLA) C, HLA-E, HLA-G with natural killer cells or dendritic cells or both is necessary for this event to occur. The presence of certain combinations of HLA-C and isoform types of immunoglobulin receptors bound to natural killer cells predispose to preeclampsia.22–25 The intervillous blood flow seems to begin by the 7th to 8th week of pregnancy, by connections between spiral arteries and lakes formed in the wall of the implanted blastocyst.26 A tamponade is formed early by the trophoblast that protects the embryo from high oxygen concentrations. Editorial

Preeclampsia: Vascular Pathophysiological Mechanism and the Basis for Early Diagnosis and Treatment