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Titolo:
Hypertension in pregnancy
Autore:
Pipkin, FB; Roberts, JM;
Indirizzi:
Univ Nottingham, Sch Human Dev, Nottingham NG7 2RD, England Univ Nottingham Nottingham England NG7 2RD , Nottingham NG7 2RD, England
Titolo Testata:
JOURNAL OF HUMAN HYPERTENSION
fascicolo: 10-11, volume: 14, anno: 2000,
pagine: 705 - 724
SICI:
0950-9240(200010/11)14:10-11<705:HIP>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; HUMAN-ENDOTHELIAL-CELLS; ANGIOTENSIN-II BINDING; FREE FATTY-ACIDS; METHYLENETETRAHYDROFOLATE REDUCTASE POLYMORPHISM; EXTRACELLULAR FLUID VOLUMES; PREECLAMPTIC WOMEN INCREASE; PLASMA CELLULAR FIBRONECTIN; HEALTHY NULLIPAROUS WOMEN; LIPOPROTEIN-LIPASE GENE;
Keywords:
pregnancy; hypertension; pre-eclampsia; gestational hypertension;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
244
Recensione:
Indirizzi per estratti:
Indirizzo: Pipkin, FB Univ Nottingham Hosp, Dept Obstet & Gynaecol, Nottingham NG7 2UH, England Univ Nottingham Hosp Nottingham England NG7 2UH 2UH, England
Citazione:
F.B. Pipkin e J.M. Roberts, "Hypertension in pregnancy", J HUM HYPER, 14(10-11), 2000, pp. 705-724

Abstract

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 halfthe 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, similiar features are found in association with non-hypertensive fetal growth restriction. Prospective studieshave suggested a hyperdynamic circulation in early pregnancy, with cardiacoutput 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 PR, perhaps through a variantof the hypoxia-reperfusion phenomenon in the developing intervillous spaces. Such early changes might then lead to the clinically-evident syndrome insusceptible women. PE is a protean, multisystem, multifactorial disease, the causes of which are only slightly less enigmatic than a decade ago.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 22:39:23