Preeclampsia, a systemic syndrome of pregnancy clinically characterized by new onset of proteinuria and hypertension, is associated with significant morbidity and mortality to both mothers and fetuses. The pathogenesis of preeclampsia has been enigmatic; this review will focus on understanding the origins of this disorder. Preeclampsia originates in the placenta, starting with inadequate cytotrophoblast invasion and ending with widespread maternal endothelial dysfunction. Production of placental anti-angiogenic factors, specifically soluble fms-related tyrosine kinase 1 and soluble endoglin, have been shown to be upregulated in preeclampsia. These placental anti-angiogenic factors are released into the maternal circulation; their actions disrupt the maternal endothelium and result in hypertension, proteinuria, and the other systemic manifestations of preeclampsia. The molecular basis for placental dysregulation of these pathogenic factors remains unknown, remains unknown. Hypoxia is likely an important regulator. Other factors such as alterations in the renin-angiotensin-aldosterone axis, immune maladaption, excessive shedding of trophoblast debris, oxidative stress, and genetic factors likely contribute to the pathogenesis of the abnormal placentation. As of 2009, the only successful treatment for preeclampsia is delivery. No definitive preventive strategies have been identified. However, several of the recent observations related to phenotypic causality provide stimuli for the development of novel therapies.

Preeclampsia: the role of angiogenic factors in its pathogenesis.

Physiologic changes during normal pregnancy and delivery.

Background: Oxygen plays a central role in human placental pathologies including preeclampsia, a leading cause of fetal and maternal death and morbidity. Insufficient uteroplacental oxygenation in preeclampsia is believed to be responsible for the molecular events leading to the clinical manifestations of this disease. Design: Using high-throughput functional genomics, we determined the global gene expression profiles of placentae from high altitude pregnancies, a natural in vivo model of chronic hypoxia, as well as that of first-trimester explants under 3 and 20% oxygen, an in vitro organ culture model. We next compared the genomic profile from these two models with that obtained from pregnancies complicated by preeclampsia. Microarray data were analyzed using the binary tree-structured vector quantization algorithm, which generates global gene expression maps. Results: Our results highlight a striking global gene expression similarity between 3% O2-treated explants, high-altitude placentae, and importan...

Molecular Evidence of Placental Hypoxia in Preeclampsia

http://facpub.stjohns.edu/%7Esees/Pcotherapy/HTNurg.pdf

The Diagnosis and Management of Hypertensive Crises

How I treat thrombocytopenia in pregnancy

Hypertension in pregnancy is still a leading cause of morbidity and mortality in mother and fetus. This review of the literature from 1991 to 1992 focuses on research relating to the causes of preeclampsia and the pathogenesis of the marked vasoconstriction so characteristic of this disease. Reports hypothesizing primary roles for endothelial cell dysfunction, aberrations in prostaglandin synthesis, fatty acid and antioxidant metabolism, as well as for dietary calcium deficiency and the renin-angiotensin system are analyzed; articles regarding clinical trials whose origins derive from some of these hypotheses, such as low-dose aspirin and calcium supplementation to prevent preeclampsia, are appraised. The review concludes by examining several controversies regarding management of pregnant women with chronic hypertension, including the proper way to measure blood pressure in pregnancy, the diastolic level at which treatment with antihypertensive medications should commence, and the choice of drugs that are safe and preferable for use during gestation.

Hypertension in pregnancy.

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Hypertension in pregnancy.