Introduction Preeclampsia (PE) is a major complication of pregnancy that could lead to maternal and fetal morbidity and mortality. The pathophysiological mechanisms of PE are not completely understood, but recent research has begun to unravel some of the potential mechanisms. Areas covered Genetic polymorphisms and altered maternal immune response may cause impaired remodeling of the spiral arteries; a potential early defect in PE. Inadequate invasion of cytotrophoblasts into the decidua leads to reduced uteroplacental perfusion pressure (RUPP) and placental ischemia/hypoxia. Placental ischemia causes the release of biologically active factors such as anti-angiogenic factors, inflammatory cytokines, reactive oxygen species, hypoxia-inducible factors, and angiotensin II receptor autoantibodies. These vasoactive factors could cause systemic vascular endotheliosis and consequent increase in vascular resistance and blood pressure, glomerular endotheliosis causing proteinuria, cerebrovascular endotheliosis causing cerebral edema, seizures and visual disturbances, and hepatic endotheliosis which may contribute to the manifestations of HELLP syndrome. PE-associated vascular endotheliosis causes a decrease in vasodilator mediators such as nitric oxide, prostacyclin and endothelium-derived hyperpolarizing factor, an increase in vasoconstrictors such as endothelin-1, angiotensin II and thromboxane A2, and enhanced mechanisms of vascular smooth muscle contraction such as intracellular Ca2+, protein kinase C and Rho-kinase. Changes in matrix metalloproteinase activity and extracellular matrix cause vascular remodeling and further vasoconstriction. Expert opinion Some of the genetic, immune and vasoactive factors involved in vascular endotheliosis could be used as biomarkers for early detection, and as potential targets for prevention and treatment of PE.

Ensuring the safety of the blood supply connects politics and science. The business and service sectors share responsibility for the collection and processing of blood donations, and government agencies perform regulatory and surveillance roles. The onset of the AIDS epidemic has challenged the interface among these systems, leading to widespread fears about compromised safety of the blood supply. Because of public concern about blood-supply decisions made in the 1980s, developed countries in the 1990s established reimbursement programs for persons with transfusion-acquired viral infections from blood or blood products, adopted diagnostic tests and procedures that improved the safety of the blood supply, and held criminal judicial investigations of government officials and industry leaders accused of delaying implementation of potential blood-safety measures. In contrast, developing countries continue to struggle with blood-supply safety issues. This paper summarizes the current status of these safety concerns in developed countries, where viral transmission from contaminated blood or blood products is extremely rare, and in developing countries, where up to 10% of HIV infections result from transfusion of blood or blood products.

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