ライフサイエンスコーパス: eclampsia

1 hypertension and 133 [67.2%] of 198 for pre-eclampsia).

2 (usual care) in women with late preterm pre-eclampsia.

3 ced the time to clinical confirmation of pre-eclampsia.

4 how a significant reduction in recurrent pre-eclampsia.

5 ism for the enhanced oxidative stress in pre-eclampsia.

6 00 women die annually from pre-eclampsia and eclampsia.

7 requency, large-effect risk variants for pre-eclampsia.

8 icated by a composite outcome of SGA and pre-eclampsia.

9 entified in people with hypertension and pre-eclampsia.

10 ic KIR B genes protect Europeans against pre-eclampsia.

11 of cytotoxic drugs, autoimmune disorders, or eclampsia.

12 he risks of gestational hypertension and pre-eclampsia.

13 l outcomes among Chinese population with pre-eclampsia.

14 eight, pregnancy loss or miscarriage, or pre-eclampsia.

15 ntitis was significantly associated with pre-eclampsia.

16 is accentuated by multiple gestation and pre-eclampsia.

17 corin and ANP function may contribute to pre-eclampsia.

18 mic angiogenic imbalance, accentuated by pre-eclampsia.

19 sure and proteinuria, characteristics of pre-eclampsia.

20 rnal blood to the placenta, but fails in pre-eclampsia.

21 ing intra-uterine growth restriction and pre-eclampsia.

22 edema-the clinical signs of preeclampsia and eclampsia.

23 am molecular defect(s) may contribute to pre-eclampsia.

24 indeed contribute to the hypertension of pre-eclampsia.

25 significantly lower in women with severe pre-eclampsia.

26 inity-purified AT(1)-AAs from women with pre-eclampsia.

27 bute to some of the maternal symptoms of pre-eclampsia.

28 branes (PPROM), placental abruption, and pre-eclampsia.

29 n placenta and predisposes the mother to pre-eclampsia.

30 could result in the maternal syndrome of pre-eclampsia.

31 aquaporin-4 protein in brain and its role in eclampsia.

32 acutely and excessively elevated, as during eclampsia.

33 fetal growth restriction associated with pre-eclampsia.

34 e of birth and the development of severe pre-eclampsia.

35 factor for gestational hypertension and pre-eclampsia.

36 719 (7.3%) with HDP and 324 (3.3%) with pre-eclampsia.

37 ated PE leads to life threatening condition, eclampsia.

38 inogen (AGT) may have a critical role in pre-eclampsia.

39 ies, particularly in FGR associated with pre-eclampsia.

40 ciated with gestational hypertension and pre-eclampsia.

41 d and assessed 1035 women with suspected pre-eclampsia.

42 the angiogenic imbalance observed during pre-eclampsia.

43 rigin from the placenta is a hallmark of pre-eclampsia.

44 ension and 1.11 (95% CI: 0.63, 1.93) for pre-eclampsia.

45 rm maternal and fetal risks conferred by pre-eclampsia.

46 cer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin membership (0.93 [

47 0 November 2017, there were 2,692 women with eclampsia (0.5%).

48 54 (95% CI, 1.39-1.70) after preeclampsia or eclampsia, 1.51 (95% CI, 1.27-1.80) after GH vs no HDP,

49 re units during an average 2 years were: pre-eclampsia, 1.78 (95% CI 1.52-2.08); gestational hyperten

50 fer was associated with a higher risk of pre-eclampsia (16 of 512 [3.1%] vs four of 401 [1.0%]; RR 3.

51 ) or intramuscular magnesium sulfate for pre-eclampsia (198 [1%]), of whom most accepted treatment (1

52 -0.51 and -3.8; 95% CI: -5.0, -2.5), and pre-eclampsia (-3.2; 95% CI: -4.2, -2.2 and -4.0; 95% CI: -5

53 nety-five (0.99%) women developed severe pre-eclampsia, 47.6% were non-European immigrants, 16.3% wer

54 d postpartum haemorrhage (70% each), and pre-eclampsia (56%).

55 Remodeling is impaired during pre-eclampsia, a disease of pregnancy that results in matern

56 g normal pregnancy, is down regulated in pre-eclampsia, a human pregnancy disorder associated with po

57 rtery remodelling has been implicated in pre-eclampsia, a major complication of pregnancy, for a long

58 One-third of the deaths are caused by pre-eclampsia, a syndrome arising from defective placentatio

59 e general population had a lower risk of pre-eclampsia-a common pregnancy complication related to hig

60 e (SGA) birth, gestational diabetes, and pre-eclampsia according to density of fruits and vegetables

61 gnesium sulfate availability and the rate of eclampsia across sites (p = 0.12).

62 lacentas from pregnancies complicated by pre-eclampsia (adjusted odds ratio (aOR) 1.46, 95% CI: 1.12-

63 Pre-eclampsia affects 2% to 8% of all pregnancies worldwide

64 Pre-eclampsia affects 3-5% of pregnancies and is traditional

65 Pre-eclampsia affects approximately 5% of pregnancies and re

66 The increased risk of pre-eclampsia after frozen blastocyst transfer warrants furt

67 m birth, PPROM, placental abruption, and pre-eclampsia aggregate in families, which may be explained

68 B) RNA was detected in 6.1% of cases of pre-eclampsia and 2.2% of other pregnancies.

69 ting all pregnant women who diagnosed as pre-eclampsia and delivered from 2005 to 2014.

70 of breast cancer was noted for maternal pre-eclampsia and eclampsia (0.48 [0.30-0.78]) and twin memb

71 might account for the high prevalence of pre-eclampsia and eclampsia in low-income countries.

72 Participants with previous pre-eclampsia and eclampsia received 500 mg calcium or place

73 2 000 and 77 000 women die annually from pre-eclampsia and eclampsia.

74 Pre-eclampsia and fetal growth restriction arise from disord

75 ociated with gestational hypoxia such as pre-eclampsia and fetal growth restriction.

76 y as a critical mechanistic link between pre-eclampsia and fetal growth restriction.

77 rpins common pregnancy disorders such as pre-eclampsia and fetal growth restriction.

78 eview is to determine the association of pre-eclampsia and future cardiovascular risk and to explore

79 ensive disorders of pregnancy, including pre-eclampsia and gestational hypertension (GHTN).

80 ted, and we estimated the RR (95% CI) of pre-eclampsia and GHTN with log-binomial regression using ge

81 top Hypertension (DASH) with the risk of pre-eclampsia and GHTN.

82 cause maternal mortality or major morbidity (eclampsia and hysterectomy).

83 placental structural changes leading to pre-eclampsia and impaired nutrient transport causing low bi

84 cated in pathological conditions such as pre-eclampsia and intra-uterine growth retardation.

85 f the feto-maternal interface results in pre-eclampsia and intrauterine growth retardation.

86 atments will hasten our understanding of pre-eclampsia and is an effort much needed by the women and

87 impaired in women who eventually develop pre-eclampsia and it occurs before the development of the cl

88 The large variation in eclampsia and maternal and neonatal fatality from hypert

89 a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk fact

90 Women with preeclampsia/eclampsia and postpartum acute systemic infection had th

91 Whilst eclampsia/pre-eclampsia and preterm gestations (33-36 weeks) were pred

92 men to test the association of them with pre-eclampsia and quantitative traits relevant for the disea

93 escribe the incidence and characteristics of eclampsia and related complications from hypertensive di

94 ed by the placenta in the development of pre-eclampsia and review novel therapeutic strategies direct

95 the prediction of both preterm and term pre-eclampsia and SGA.

96 nancy and investigated associations with pre-eclampsia and small-for-gestational-age (SGA) birth, whi

97 udies identify a genetic mouse model for pre-eclampsia and suggest that 2-ME may have utility as a pl

98 nosis, risk factors, and pathogenesis of pre-eclampsia and the present status of its prediction, prev

99 lications, including preterm and twin birth, eclampsia and toxemia, shorter period of breastfeeding,

100 ncy had been complicated by pre-eclampsia or eclampsia and who were intending to become pregnant.

101 it occurs more frequently in women with pre-eclampsia and/or multiple gestation.

102 tational hypertension [GH], preeclampsia, or eclampsia) and 1.81 (95% CI, 1.44-2.27) after GH vs no H

103 The presence or absence of mHTN (e.g., pre-eclampsia) and infant factors (birthweight, gestational

104 iated with endothelial damage (preeclampsia, eclampsia, and HELLP syndrome), and postoperative compli

105 r pregnancy-related syndromes: preeclampsia, eclampsia, and hemolysis, elevated liver enzymes, low pl

106 utcomes (APOs)-including pre-term birth, pre-eclampsia, and intrauterine growth restriction-are commo

107 ated preterm births include pre-eclampsia or eclampsia, and intrauterine growth restriction.

108 us maternal complications, including stroke, eclampsia, and organ failure.

109 , twin membership, maternal pre-eclampsia or eclampsia, and other factors.

110 Our primary endpoint was pre-eclampsia, and our main secondary endpoints were low bir

111 eart failure, hypertension in pregnancy, pre-eclampsia, and pre-term delivery; there were no differen

112 ses such as emphysema, spontaneous abortion, eclampsia, and several forms of cancer.

113 ncentrations occurs in normal pregnancy, pre-eclampsia, and SGA pregnancies.

114 Cesarean delivery, preeclampsia/eclampsia, and spontaneous abortion were also evaluated.

115 ociated with cesarean delivery, preeclampsia/eclampsia, and spontaneous abortion.

116 Oxidative stress could play a part in pre-eclampsia, and there is some evidence to suggest that vi

117 make a diagnosis in women with suspected pre-eclampsia, and whether this approach reduced subsequent

118 c events (aOR: 2.4; 95% CI: 2.0 to 2.9), pre-eclampsia (aOR: 1.5; 95% CI: 1.3 to 1.7), and placenta p

119 trauterine growth restriction (IUGR) and pre-eclampsia are associated with a greater degree of tropho

120 In conclusion, FGR and pre-eclampsia are associated with T-cell infiltration of the

121 Women with a history of pre-eclampsia are at increased risk of future cardiovascular

122 Because women who develop eclampsia are in general normotensive and asymptomatic p

123 Although algorithms to predict pre-eclampsia are promising, they have yet to become validat

124 Fetal growth restriction (FGR) and pre-eclampsia are severe, adverse pregnancy outcomes.

125 Neurologic complications of eclampsia are thought to be similar to hypertensive ence

126 , including gestational hypertension and pre-eclampsia, are common obstetric complications associated

127 wth restriction of the fetus (IUGR), and pre-eclampsia arose in ten (23%).

128 wo-fold higher risk of developing severe pre-eclampsia as compared to European-born women, one-fifth

129 The adjusted risk ratio for eclampsia associated with nimodipine, as compared with m

130 assessing coverage in the literature of pre-eclampsia-associated genes.

131 The patient was admitted with pre-eclampsia at 31 full weeks and 5 days, and 16 h later a

132 s and older who presented with suspected pre-eclampsia between 20 weeks and 0 days of gestation and 3

133 cations include gestational diabetes and pre-eclampsia, both of which are associated with long-term m

134 sted fertilization increases the risk of pre-eclampsia, but still result in live births.

135 pregnancy have not shown a reduction in pre-eclampsia, but the effect in women with diabetes is unkn

136 gnostic accuracy in women with suspected pre-eclampsia, but we remain uncertain of the effectiveness

137 expression by decidual cells to promote pre-eclampsia by interfering with local vascular transformat

138 in the trial who received a diagnosis of pre-eclampsia by their treating clinicians.

139 mortality, fetal mortality, preeclampsia or eclampsia, caesarean sections, non-delivery-related admi

140 When left untreated, pre-eclampsia can be lethal, and in low-resource settings, t

141 A third of eclampsia cases (33.2%; n = 894) occurred in women under

142 We genotyped 467 pre-eclampsia cases and 3,854 controls and found an excess o

143 n 4067 women, with 998 maternal deaths, 2692 eclampsia cases, and 681 hysterectomies.

144 om the Community-Level Interventions for Pre-eclampsia (CLIP) cluster randomised controlled trials in

145 of the Community-Level Interventions for Pre-eclampsia (CLIP) cluster randomised trials.

146 n Africa had an increased risk of severe pre-eclampsia compared to European-born mothers (aOR 2.53, 9

147 The primary outcome was pre-eclampsia, defined as gestational hypertension and prote

148 ional hypertension plus proteinuria or a pre-eclampsia-defining complication.

149 The median time to pre-eclampsia diagnosis was 4.1 days with concealed testing

150 Rates of pre-eclampsia did not differ between vitamin (15%, n=57) and

151 = 186; 3.47/10,000 deliveries) of women with eclampsia died, and a further 51 died from other complic

152 However, pre-eclampsia does not develop in all women with high sFLT-1

153 The incidence of HDP and pre-eclampsia doubled when assessed on a per-woman basis: 15

154 ncy, and one mother with SPKTx developed pre-eclampsia during both pregnancies.

155 normotensive, gestational hypertension, pre-eclampsia, eclampsia, pre-eclampsia superimposed on chro

156 ong postdelivery women with a history of pre-eclampsia/eclampsia (PEE).

157 Pre-eclampsia/eclampsia are leading causes of maternal morta

158 s were postpartum haemorrhage and severe pre-eclampsia/eclampsia.

159 rimary composite outcome was at least one of eclampsia, emergency hysterectomy, and maternal death.

160 reviously implicated in hypertension and pre-eclampsia, exhibits a similar geographic distribution an

161 In pre-eclampsia, expression of the Notch ligand JAG1 was absen

162 ed in adverse obstetric outcomes such as pre-eclampsia, fetal growth restriction, and preterm birth.

163 The RR (95% CI) of pre-eclampsia for women in the highest quintile of the DASH

164 women identified as at increased risk of pre-eclampsia from 25 hospitals.

165 randomisation in women with late preterm pre-eclampsia from 34 to less than 37 weeks' gestation and a

166 ur; breech presentation; PROM, eclampsia/pre-eclampsia; gestation 33-36 weeks; gestation 41+ weeks; o

167 t gain and subsequently increase risk of pre-eclampsia, gestational diabetes mellitus, hypertension d

168 Pre-eclampsia, gestational hypertension, and small-for-gesta

169 c hypertension and superimposed preeclampsia/eclampsia had high risk for future diseases.

170 Low birthweight, pre-term birth and pre-eclampsia have been associated with maternal periodontit

171 e is experienced by 1 in 172 women; cases of eclampsia have decreased during the audit; there were de

172 disorders with features of TMA (preeclampsia/eclampsia; hemolysis elevated liver enzymes low platelet

173 omplications during pregnancy (preeclampsia, eclampsia, hemorrhage, and hyperemesis).

174 ogical symptoms are often diagnosed with pre-eclampsia; however, a range of other causes must also be

175 wn to reduce the serious consequences of pre-eclampsia; however, the effect of calcium supplementatio

176 Acute hypertension, eclampsia, immunosuppressive medication, infection or au

177 for the high prevalence of pre-eclampsia and eclampsia in low-income countries.

178 tiplatelet agents, for the prevention of pre-eclampsia in pregnancy.

179 tween maternal place of birth and severe pre-eclampsia in the PreCARE cohort of pregnant women in Par

180 vitamin C and vitamin E does not prevent pre-eclampsia in women at risk, but does increase the rate o

181 th suspected pre-eclampsia to documented pre-eclampsia in women enrolled in the trial who received a

182 vitamins C and E did not reduce risk of pre-eclampsia in women with type 1 diabetes.

183 th vitamins C and E reduced incidence of pre-eclampsia in women with type 1 diabetes.

184 We show here that key features of pre-eclampsia, including hypertension, proteinuria, glomerul

185 Nigeria [7.1%]; p < 0.001), followed by pre-eclampsia (India [3.8%], Nigeria [3.0%], Pakistan [2.4%]

186 leted using data from 1,300 women in the Pre-eclampsia Integrated Estimate of RiSk (fullPIERS) datase

187 of curative treatment, the management of pre-eclampsia involves stabilisation of the mother and fetus

188 Pre-eclampsia is a common pregnancy disorder that is a major

189 Pre-eclampsia is a complication of pregnancy that is associa

190 Pre-eclampsia is a major cause of maternal mortality (15-20%

191 Pre-eclampsia is a multisystem placentally mediated disease,

192 Pre-eclampsia is a severe hypertensive disorder of pregnancy

193 In conclusion, the genetic risk for pre-eclampsia is likely complex even in a population isolate

194 cance, as the downregulation of HBEGF in pre-eclampsia is likely to be a contributing factor leading

195 of PlGF testing in women with suspected pre-eclampsia is supported by the results of this study.

196 An effective treatment of pre-eclampsia is unavailable owing to the poor understanding

197 ptor 1 secreted from the placenta causes pre-eclampsia-like features by antagonizing vascular endothe

198 2-ME ameliorates all pre-eclampsia-like features without toxicity in the Comt(-/-

199 female mice lacking eNOS aggravates the pre-eclampsia-like phenotype induced by increased sFlt-1.

200 techol-O-methyltransferase (COMT) show a pre-eclampsia-like phenotype resulting from an absence of 2-

201 tric oxide exacerbates the sFlt1-related pre-eclampsia-like phenotype through activation of the endot

202 associated with adverse outcomes such as pre-eclampsia, low infant birth weight, and later-life adipo

203 th, placental weight >= 600 g, eclampsia/pre-eclampsia, maternal age >= 35 and oligohydramnios.

204 significance): multiple birth; eclampsia/pre-eclampsia; maternal age 40-44 years; placental weight 60

205 Thus, our studies indicate that pre-eclampsia may be a pregnancy-induced autoimmune disease

206 ' gestation) prevents the development of pre-eclampsia METHODS: We did a multicountry, parallel arm,

207 Variants predisposing to pre-eclampsia might be under negative evolutionary selection

208 m birth (<37 weeks), growth restriction, pre-eclampsia, miscarriage and/or stillbirth.

209 35-39 years; oligohydramnios; eclampsia/pre-eclampsia; mother's age 30-34 years; birthweight <2,000

210 .8] vs 16.9 [10.4-19.1], p=0.04; preterm pre-eclampsia n=11, 23.1 [11.2-30.9] vs 17.2 [9.8-19.1], p=0

211 t the time of disease presentation (term pre-eclampsia n=14, median 22.2 ng/mL [IQR 15.1-39.8] vs 16.

212 h gestational hypertension (n = 496) and pre-eclampsia (n = 1804) were identified from the Internatio

213 ification of Diseases, Ninth Revision codes: eclampsia (n=154), severe preeclampsia (n=1,180), mild p

214 tension and obesity; a family history of pre-eclampsia, nulliparity or multiple pregnancies; and prev

215 Pre-eclampsia occurred in 69 (23%) of 296 participants in th

216 -section, gestational diabetes, preeclampsia/eclampsia or be in the third trimester (P <= 0.01).

217 recent pregnancy had been complicated by pre-eclampsia or eclampsia and who were intending to become

218 ons for indicated preterm births include pre-eclampsia or eclampsia, and intrauterine growth restrict

219 ylstilbestrol, twin membership, maternal pre-eclampsia or eclampsia, and other factors.

220 in excessive dNK inhibition, the risk of pre-eclampsia or growth restriction is increased.

221 are correlated with low birth weight and pre-eclampsia or high birth weight and obstructed labor, the

222 tus and required delivery as a result of pre-eclampsia or hypertension were randomly assigned (1:1),

223 on for induction of labour in women with pre-eclampsia or hypertension.

224 ty or multiple pregnancies; and previous pre-eclampsia or intrauterine fetal growth restriction.

225 l outcomes included in-hospital arrhythmias, eclampsia or preeclampsia, congestive heart failure (CHF

226 Blood samples from women with pre-eclampsia or SGA were analysed from the time of disease

227 ertility therapies (p = 0.0004), and had pre-eclampsia (p = 0.001).

228 encoding the C2 epitope associates with pre-eclampsia [P = 0.0318, odds ratio (OR) = 1.49].

229 e levels were significantly decreased in pre-eclampsia patients compared to normal pregnant women, po

230 Pre-eclampsia (PE) and gestational diabetes mellitus (GDM) a

231 terature and determine the prevalence of pre-eclampsia (PE) in women with PPCM.

232 nce of gestational hypertension (GH) and pre-eclampsia (PE) is increasing.

233 The primary outcome was a composite of pre-eclampsia (PE), birth of a small-for-gestational-age (SG

234 cium with gestational hypertension (GH), pre-eclampsia (PE), caesarean section (CS), preterm birth (P

235 Placental RAS is increased in pre-eclampsia (PE), characterised by placental dysfunction a

236 Pre-eclampsia (PE), which affects approximately 8% of first

237 al pregnancy and in increased amounts in pre-eclampsia (PE), which have proinflammatory and antiangio

238 lance has not been fully investigated in pre-eclampsia (PE).

239 sms that facilitate the emergence of the pre-eclampsia phenotype in women are still unknown.

240 dotheliosis (a classical renal lesion of pre-eclampsia), placental abnormalities and small fetus size

241 There was a lower risk of pre-eclampsia plus SGA combined (13.6%) at 25(OH)D concentra

242 site variants that were enriched in the pre-eclampsia pools compared to reference data, and genotype

243 ecent studies have shown that women with pre-eclampsia possess autoantibodies, termed AT(1)-AAs, that

244 ve, gestational hypertension, pre-eclampsia, eclampsia, pre-eclampsia superimposed on chronic hyperte

245 Whilst eclampsia/pre-eclampsia and preterm gestations (33-36 we

246 , multiple birth, placental weight >= 600 g, eclampsia/pre-eclampsia, maternal age >= 35 and oligohyd

247 bstructed labour; breech presentation; PROM, eclampsia/pre-eclampsia; gestation 33-36 weeks; gestatio

248 f statistical significance): multiple birth; eclampsia/pre-eclampsia; maternal age 40-44 years; place

249 age >= 45 and 35-39 years; oligohydramnios; eclampsia/pre-eclampsia; mother's age 30-34 years; birth

250 Because pre-eclampsia predisposes mothers to cardiovascular disease

251 gnancy-associated phenotype that encompassed eclampsia, preeclampsia, fetal/neonatal deaths, and smal

252 increased risk of gestational diabetes, pre-eclampsia, preterm birth, instrumental and caesarean bir

253 Participants with previous pre-eclampsia and eclampsia received 500 mg calcium or placebo daily from

254 , only 77% of women with severe preeclampsia/eclampsia received magnesium sulphate and 67% with antep

255 factors, but the diagnostic criteria of pre-eclampsia remain unclear, with no known biomarkers.

256 y of PPCM, and why it is associated with pre-eclampsia, remain unknown.

257 m birth, PPROM, placental abruption, and pre-eclampsia, respectively).

258 m birth, PPROM, placental abruption, and pre-eclampsia, respectively).

259 ociated with 1.1% and 1.4% reductions in pre-eclampsia risk compared with lower densities, respective

260 re pregnancy to 20 weeks' gestation, the pre-eclampsia risk was 30 (21%) of 144 versus 47 (32%) of 14

261 r during pregnancy (RR 1.28, 1.19-1.36), pre-eclampsia (RR 1.32, 1.20-1.45), prepregnancy maternal an

262 hesis has obvious implications regarding pre-eclampsia screening, diagnosis and therapy.

263 Strategies to prevent eclampsia should be informed by local data.

264 dently adjudicated severe or early-onset pre-eclampsia, small-for-gestational-age infant (birthweight

265 mediated pregnancy complications (severe pre-eclampsia, small-for-gestational-age infants, and placen

266 We sought to determine whether pre-eclampsia, spontaneous preterm birth or the delivery of

267 Data on eclampsia, stroke, admission to intensive care with a hy

268 Nearly 1 in 5 (17.9%) women with eclampsia, stroke, or a hypertensive disorder of pregnan

269 with any significant change in the rates of eclampsia, stroke, or maternal death or intensive care a

270 ternal and infant health outcomes, including eclampsia, stroke, stillbirth, preterm birth, and low bi

271 -analyses of low-dose aspirin to prevent pre-eclampsia suggest that the incidence of preterm birth mi

272 hypertension, pre-eclampsia, eclampsia, pre-eclampsia superimposed on chronic hypertension, and chro

273 concentrations were higher in women with pre-eclampsia than in controls at the time of disease presen

274 In women with late preterm pre-eclampsia, the optimal time to initiate delivery is uncl

275 B was implicated in pregnancy-associated pre-eclampsia, the regulation of NK-B synthesis and function

276 dged form in the maternal circulation in pre-eclampsia-the hypertensive crisis of pregnancy that thre

277 e discussed with women with late preterm pre-eclampsia to allow shared decision making on timing of d

278 he time from presentation with suspected pre-eclampsia to documented pre-eclampsia in women enrolled

279 Pre-eclampsia (typically characterized by new-onset hyperten

280 In patients with pre-eclampsia, uterine Corin messenger RNA and protein level

281 Rates of eclampsia varied approximately 7-fold between sites (ran

282 s 1.66 (95% CI: 1.42, 1.94) and that for pre-eclampsia was 1.57 (95% CI: 1.46, 1.70) per BMI z score.

283 The prevalence of pre-eclampsia was 3.8%, and 10.7% of infants were SGA.

284 Suspected pre-eclampsia was defined as new-onset or worsening of exist

285 gestation) or gestational (>=20 weeks); pre-eclampsia was gestational hypertension plus proteinuria

286 shed one of the earliest descriptions of pre-eclampsia was incorrectly stated to be 1637, which is ac

287 Toxemia of pregnancy or pre-eclampsia was observed in 23% of pregnancies postKTx and

288 11.6% in Pakistan, and 16.8% in Mozambique; eclampsia was rare (<0.5%).

289 Pre-eclampsia was reported in 495 (2.9%) pregnancies and GHT

290 The incidence of pre-eclampsia was similar in treatment placebo groups (15% [

291 nts in individuals with hypertension and pre-eclampsia were defective in PCSK6-mediated activation.

292 es of small-for-gestational age (SGA) or pre-eclampsia were matched with healthy controls.

293 Women experiencing severe pre-eclampsia were more likely to be from Sub-Saharan Africa

294 ible, declined to participate, had impending eclampsia, were in active labour, or had a combination o

295 red in both fetal growth restriction and pre-eclampsia, whereas CD79alpha(+) B-cell infiltration was

296 sub-Saharan Africans and Europeans from pre-eclampsia, whereas in both populations, the KIR AA genot

297 ed risks of gestational hypertension and pre-eclampsia, whereas normalizing BMI from childhood to con

298 The primary endpoint was pre-eclampsia, which we defined as gestational hypertension

299 Preeclampsia or eclampsia with onset before or after 34 weeks of gestati

300 common (1.7%) and were primarily due to pre-eclampsia with severe features.