Preeclampsia

Pauli, Jaimey M.; Repke, John T.

doi:10.1016/j.ogc.2015.01.007

Cited by 72 publications

(36 citation statements)

References 35 publications

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“…Some women with GH will subsequently progress to PE, which affects 2%–5% of pregnancies and is traditionally diagnosed by the presentation of high BP (≥ 140/90 mmHg), accompanied by proteinuria (≥ 300 mg /24 h or ≥ 1+ on a dipstick) or maternal organ dysfunction [4–8]. PE is one of the main causes of maternal and perinatal morbidity and mortality, especially in low- and middle-income countries [5, 6, 8], and predisposes mothers and fetuses to cardiovascular disease later in life [6, 7, 9–11]. Common risk factors for GH-PE include older age, first pregnancy, pre-pregnancy obesity (elevated body mass index [BMI]), multiple-fetus pregnancy, polycystic ovarian syndrome, chronic kidney disease, overt diabetes, and autoimmune disease [4–7, 12–18].…”

Section: Introductionmentioning

confidence: 99%

“…PE is one of the main causes of maternal and perinatal morbidity and mortality, especially in low- and middle-income countries [5, 6, 8], and predisposes mothers and fetuses to cardiovascular disease later in life [6, 7, 9–11]. Common risk factors for GH-PE include older age, first pregnancy, pre-pregnancy obesity (elevated body mass index [BMI]), multiple-fetus pregnancy, polycystic ovarian syndrome, chronic kidney disease, overt diabetes, and autoimmune disease [4–7, 12–18]. However, in clinical practice, these risk factors only predict 30% of women who will develop PE [6–7].…”

Section: Introductionmentioning

confidence: 99%

“…Common risk factors for GH-PE include older age, first pregnancy, pre-pregnancy obesity (elevated body mass index [BMI]), multiple-fetus pregnancy, polycystic ovarian syndrome, chronic kidney disease, overt diabetes, and autoimmune disease [4–7, 12–18]. However, in clinical practice, these risk factors only predict 30% of women who will develop PE [6–7]. The two-stage model of abnormal trophoblastic invasion during placental implantation, placental ischemia, and subsequent endothelial injury has been established as the possible etiology and pathophysiology underlying GH-PE [4, 5, 7, 12, 19, 20].…”

Section: Introductionmentioning

confidence: 99%

“…However, in clinical practice, these risk factors only predict 30% of women who will develop PE [6–7]. The two-stage model of abnormal trophoblastic invasion during placental implantation, placental ischemia, and subsequent endothelial injury has been established as the possible etiology and pathophysiology underlying GH-PE [4, 5, 7, 12, 19, 20]. Some biophysical and biochemical methods including maternal uterine artery Doppler [7, 9, 13, 19], fetal aorta intima-media thickness (aIMT) [9], and biochemical markers [12–14, 18] have been developed for detecting PE among low-risk populations.…”

Section: Introductionmentioning

confidence: 99%

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Risk of gestational hypertension-preeclampsia in women with preceding endometriosis: A nationwide population-based study

et al. 2017

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ObjectiveTo investigate the association between preceding endometriosis and gestational hypertension-preeclampsia (GH-PE).MethodsIn this nationwide population-based longitudinal study, data from 1998–2012 Taiwan National Health Insurance Research Database were used. We used ICD9-CM codes 617.X and 642.X respectively for the diagnoses of endometriosis and GH-PE, which were further confirmed by examining medical records of surgeries, blood pressure and urine protein to ensure the accuracy of the diagnoses. The study excluded women diagnosed with endometriosis at < 15 or > 45 years of age, chronic hypertension, and GH-PE prior to endometriosis. Each pregnant woman with a prior diagnosis of endometriosis was matched to 4 pregnant women without endometriosis by age. Logistic regression analysis was used to calculate odds ratios (ORs) for the risk of GH-PE with adjustment for age, occupation, urbanization, economic status and comorbidities.ResultsAmong 6,300 women with a prior endometriosis diagnosis who were retrieved from a population of 1,000,000 residents, 2,578 (40.92%) had subsequent pregnancies that were eligible for further analysis and were compared with 10,312 pregnant women without previous endometriosis. GH-PE occurred more in women with prior endometriosis as compared to those without endometriosis (3.88% vs. 1.63%, p<0.0001). Further analysis revealed prior endometriosis was associated with GH-PE (adjusted OR = 2.27; 95% CI:1.76–2.93). For danazol-treated and non-danazol-treated subgroups, the incidences of GH-PE were 3.13% (15/480) and 4.05% (85/2,098), respectively. Although the risk for subsequent GH-PE was lower (adjusted OR = 1.49; 95% CI:0.86–2.56) after receiving danazol treatment than average (adjusted OR = 2.27; 95% CI:1.76–2.93) for women with preceding endometriosis, the reduction of risk was not statistically remarkable for danazol-treated (adjusted OR = 1.49) vs. non-danazol-treated (adjusted OR = 2.48) subgroups (p heterogeneity = 0.12).ConclusionsPreceding endometriosis is an independent and significant risk factor for the occurrence of GH-PE.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Risk of gestational hypertension-preeclampsia in women with preceding endometriosis: A nationwide population-based study

et al. 2017

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“…Patients with preeclampsia have increased maternal morbidity and mortality rates. (2, 3) Treatment of preeclampsia is limited to symptomatic control and/or early termination of pregnancy. Despite decades of research, the pathogenesis underlying preeclampsia remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Expression of ADAMTS13 in Normal and Abnormal Placentae and Its Potential Role in Angiogenesis and Placenta Development

Feng

et al. 2017

ATVB

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Objective ADAMTS13 is primarily synthesized in liver. The biosynthesis and its physiological role in placenta are not known. Approach and Results We employed real time polymerase chain reaction (PCR), immunohistochemistry, and Western blotting analyses, as well as proteolytic cleavage of FRETS-VWF73 to determine ADAMTS13 expression in placenta and trophoblasts obtained from individuals with normal pregnancy and patients with severe preeclampsia. We also determined the role of ADAMTS13 in extravillous trophoblasts using a 3-(4,5-Dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay, wound scratch assay, transwell migration assay, tube formation assay, and tissue outgrowth assays. We demonstrated that full-length and proteolytically active ADAMTS13 was expressed in normal human placenta, primarily in the trophoblasts and villous core fetal vessel endothelium during pregnancy. Placental expression of ADAMTS13 mRNA, protein, and proteolytic activity was at the highest levels during the first trimester and significantly reduced at the term of gestation. Additionally, significantly reduced levels of placental ADAMTS13 expression was detected under hypoxic conditions and in patients with preeclampsia. In addition, recombinant ADAMTS13 protease stimulated proliferation, migration, invasion, and network formation of trophoblastic cells in culture. Finally, knockdown of ADAMTS13 expression attenuated the ability of tube formation in HTR-8/SVNEO cells and the extravillous trophoblast outgrowth in placental explants. Conclusions Our results demonstrate for the first time the expression of ADAMTS13 mRNA and protein in normal and abnormal placental tissues and its role in promoting angiogenesis and trophoblastic cell development. The findings support the potential role of the ADAMTS13-von Willebrand factor pathway in normal pregnancy and pathogenesis of preeclampsia.

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