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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| Vydáno v: | Journal of human hypertension Ročník 14; číslo 10-11; s. 705 - 724 |
|---|---|
| Hlavní autoři: | , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Basingstoke
Nature Publishing
01.10.2000
Nature Publishing Group |
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| ISSN: | 0950-9240, 1476-5527 |
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| 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 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. |
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| AbstractList | 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.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. 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, similiar 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, viaoxidation 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, multi- system, multifactorial disease, the causes of which are only slightly less enigmatic than a decade ago. 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. |
| Author | Roberts, JM Broughton Pipkin, F |
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| CitedBy_id | crossref_primary_10_1016_j_placenta_2006_10_004 crossref_primary_10_1053_sper_2002_29836 crossref_primary_10_1081_PRG_120024033 crossref_primary_10_1038_srep19588 crossref_primary_10_1016_S1889_1837_06_71641_5 crossref_primary_10_1056_NEJM200103223441209 crossref_primary_10_1038_ki_2008_620 crossref_primary_10_1016_j_jpsychores_2005_06_072 crossref_primary_10_1067_mob_2002_123281 crossref_primary_10_1111_j_1751_7176_2010_00288_x crossref_primary_10_1111_j_1365_3016_2006_00761_x crossref_primary_10_1016_j_ejogrb_2007_08_005 crossref_primary_10_1016_j_earlhumdev_2005_11_007 crossref_primary_10_1080_10641950701274870 crossref_primary_10_1007_s10286_023_00976_4 crossref_primary_10_1161_01_HYP_0000196731_56062_7c crossref_primary_10_1016_S0268_960X_02_00056_5 crossref_primary_10_1017_S096553951200006X crossref_primary_10_1007_s11325_016_1345_9 crossref_primary_10_1016_j_preghy_2019_11_003 crossref_primary_10_1016_j_cmpb_2024_108050 crossref_primary_10_1080_10641950701825937 crossref_primary_10_1161_HYPERTENSIONAHA_114_03530 crossref_primary_10_1515_JPM_2005_099 crossref_primary_10_2466_02_13_PR0_107_5_415_423 crossref_primary_10_1007_s10038_006_0106_1 crossref_primary_10_1016_j_biocel_2003_09_001 crossref_primary_10_1016_j_ajog_2010_01_057 crossref_primary_10_1016_j_placenta_2004_01_009 crossref_primary_10_1080_14767058_2018_1427058 crossref_primary_10_1136_fn_86_1_F4 crossref_primary_10_1016_j_ajog_2004_11_023 crossref_primary_10_1016_j_rdc_2005_04_001 crossref_primary_10_1176_appi_psy_49_5_413 crossref_primary_10_3892_mmr_2015_3414 crossref_primary_10_1016_S0212_8241_06_71755_8 crossref_primary_10_1080_14767050902866804 |
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| DOI | 10.1038/sj.jhh.1001018 |
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| Keywords | Pregnancy Human Hypertension Concomitant disease Prognosis Pregnancy disorders Pathophysiology Pathogenesis Preeclampsia Cardiovascular disease Pregnancy toxemia |
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| SubjectTerms | 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 |
| Title | Hypertension in pregnancy |
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