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Preeclampsia: Pathophysiology, Diagnosis, and Management
Abstract
Preeclampsia, a major cause of fetal and maternal morbidity and mortality, may be difficult to distinguish clinically from other hypertensive disorders of pregnancy. Signs helpful in its diagnosis include presentation during late gestation in a nullipara with edema and proteinuria, and one or more of the following: hemoconcentration, hypoalbuminemia, liver function and/or coagulation abnormalities, and increased urate levels. Measures that may prove useful in differentiating preeclampsia from less dangerous forms of hypertension are decreased antithrombin III levels, increments in serum iron and carboxyhemoglobin, and decreases in urinary calcium. Major pathophysiological features of preeclampsia are decreased cardiac output, pulmonary capillary wedge pressure, and plasma volume; and marked increases in peripheral vascular resistance, as well as exaggerated pressor responses to endogenous angiotensin II and catecholamines. Renal hemodynamics decrease, in part as a result of a characteristic morphological lesion in glomeruli ("endotheliosis"), and there may be increased vascular permeability leading to albumin loss from the intravascular space. When gestation is advanced, termination is the treatment of choice; when temporization is required, several antihypertensive medications whose safety and efficacy have been tested in pregnant women are available. Magnesium sulfate remains the drug of choice for impending convulsions (the eclamptic phase of the disease). Finally, the etiology of preeclampsia remains unknown, but a popular theory suggests that alterations in prostaglandin metabolism may be responsible for the hypertension and coagulopathy in this disorder. In this respect, prophylactic treatment with low doses of aspirin, which decrease platelet thromboxane production but spare endothelial prostacyclin release, may decrease the incidence of preeclampsia in "high-risk" populations.
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“A similar pattern is observed for VEGF, stimulating angiogenesis and promoting capillary permeability,29 leading to expansion of the interstitium.30, 31”
From Hypoalbuminemia: Pathogenesis and Clinical Significance (2019) · cites this paper as [31]
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Metadata
- Authors
- Lindheimer, M. D., & Katz, A. I.
- Affiliations
- University of Chicago (US)
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 1989-02
- Volume
- 40
- Issue
- 1
- Pages
- 233-250
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- OpenAlex
- W2115403364
- Cited by
- 128
- References
- 47
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 6 · 2020: 5 · 2019: 5 · 2018: 8 · 2017: 1 · 2016: 11 · 2015: 2 · 2014: 7 · 2013: 6 · 2012: 4
- FWCI
- 12.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-24498)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Clinical Neurology › Neurological Complications and Syndromes
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy-related medical research
- Keywords
- preeclampsia, hypertensive disorders of pregnancy, pathophysiology, proteinuria, endotheliosis, antithrombin III, magnesium sulfate, eclampsia, antihypertensive drugs in pregnancy, aspirin prophylaxis, prostaglandin metabolism, thrombocytopenia, systemic vascular resistance, abortion
- MeSH terms
- Antihypertensive Agents, Diagnosis, Differential, Eclampsia, Female, Hemodynamics, Humans, Magnesium Sulfate, Pre-Eclampsia, Pregnancy, Dinoprostone
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