Hypertension in pregnancy

Hypertension arising during pregnancy remains one of the two most frequently-cited causes of maternal death in the UK. In some cases, pregnancy is unmasking underlying hypertension, which manifests itself in later life. Pregnant women who develop de novo proteinuric hypertension (pre-eclampsia, PE)...

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Veröffentlicht in:	Journal of human hypertension Jg. 14; H. 10-11; S. 705 - 724
Hauptverfasser:	Broughton Pipkin, F, Roberts, JM
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Basingstoke Nature Publishing 01.10.2000 Nature Publishing Group
Schlagworte:	Arterial hypertension. Arterial hypotension Arteries Arteriosclerosis Baroreceptors Baroreflex Biological and medical sciences Blood and lymphatic vessels Blood Pressure Cardiac Output Cardiology. Vascular system Cell activation Clinical manifestations. Epidemiology. Investigative techniques. Etiology Disease Susceptibility Diseases of mother, fetus and pregnancy Dyslipidemia Endothelial cells Endothelium, Vascular - metabolism Female Fetuses Gynecology. Andrology. Obstetrics Humans Hypertension Hypertension - etiology Hypertension - metabolism Hypertension - physiopathology Hypoxia Insulin Insulin resistance Lipids Medical sciences Metabolic syndrome Oxidative Stress Pre-eclampsia Preeclampsia Pregnancy Pregnancy Complications, Cardiovascular Pregnancy. Fetus. Placenta Prognosis Reflexes Reperfusion Risk Factors Womens health Pregnancy Human Hypertension Concomitant disease Prognosis Pregnancy disorders Pathophysiology Pathogenesis Preeclampsia Cardiovascular disease Pregnancy toxemia
ISSN:	0950-9240, 1476-5527
Online-Zugang:	Volltext
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Zusammenfassung:	Hypertension arising during pregnancy remains one of the two most frequently-cited causes of maternal death in the UK. In some cases, pregnancy is unmasking underlying hypertension, which manifests itself in later life. Pregnant women who develop de novo proteinuric hypertension (pre-eclampsia, PE) can share many risk factors with patients with the metabolic syndrome, such as obesity, dyslipidaemia and insulin resistance. However, more than half the women who develop PE remain normotensive thereafter. There is a genetic component(s) to the disease, but it is most improbable that there is a 'PE gene'. Rather, there are factors such as genetically-determined thrombophilias which are predisposers but not prerequisites. Impaired placentation is a feature, with inadequate invasion of the spiral arteries by syncytiotrophoblast and poor remodelling. However, similar features are found in association with non-hypertensive fetal growth restriction. Prospective studies have suggested a hyperdynamic circulation in early pregnancy, with cardiac output only falling in established disease. Baroreflex sensitivity is decreased in normal pregnancy, and still further decreased in established PE. Activation of endothelial cell function antedates the clinical diagnosis, and has features in common with atherosclerosis. Dyslipidaemia is common in PE and, via oxidation of susceptible lipids, may contribute to endothelial activation. Oxidative 'stress' is increased in PE, perhaps through a variant of the hypoxia-reperfusion phenomenon in the developing intervillous spaces. Such early changes might then lead to the clinically-evident syndrome in susceptible women. PE is a protean, multisystem, multifactorial disease, the causes of which are only slightly less enigmatic than a decade ago.
Bibliographie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
ISSN:	0950-9240 1476-5527
DOI:	10.1038/sj.jhh.1001018