ライフサイエンスコーパス: pre-eclampsia

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

2 chanism for the enhanced oxidative stress in pre-eclampsia.

3 ow-frequency, large-effect risk variants for pre-eclampsia.

4 indicated by a composite outcome of SGA and pre-eclampsia.

5 n identified in people with hypertension and pre-eclampsia.

6 omeric KIR B genes protect Europeans against pre-eclampsia.

7 te the risks of gestational hypertension and pre-eclampsia.

8 ernal outcomes among Chinese population with pre-eclampsia.

9 rthweight, pregnancy loss or miscarriage, or pre-eclampsia.

10 iodontitis was significantly associated with pre-eclampsia.

11 his is accentuated by multiple gestation and pre-eclampsia.

12 in corin and ANP function may contribute to pre-eclampsia.

13 ystemic angiogenic imbalance, accentuated by pre-eclampsia.

14 pressure and proteinuria, characteristics of pre-eclampsia.

15 maternal blood to the placenta, but fails in pre-eclampsia.

16 cluding intra-uterine growth restriction and pre-eclampsia.

17 stream molecular defect(s) may contribute to pre-eclampsia.

18 place of birth and the development of severe pre-eclampsia.

19 are significantly lower in women with severe pre-eclampsia.

20 affinity-purified AT(1)-AAs from women with pre-eclampsia.

21 ntribute to some of the maternal symptoms of pre-eclampsia.

22 uld indeed contribute to the hypertension of pre-eclampsia.

23 membranes (PPROM), placental abruption, and pre-eclampsia.

24 ion could result in the maternal syndrome of pre-eclampsia.

25 human placenta and predisposes the mother to pre-eclampsia.

26 precede and contribute to the development of pre-eclampsia.

27 abour, small for gestational age infants, or pre-eclampsia.

28 of the immune system in the pathogenesis of pre-eclampsia.

29 ing plasma extravasation in diseases such as pre-eclampsia.

30 evated in pregnancy-induced hypertension and pre-eclampsia.

31 lacental insufficiency and the occurrence of pre-eclampsia.

32 as been implicated in the pathophysiology of pre-eclampsia.

33 ms of circulating inhibin A and activin A in pre-eclampsia.

34 ther evidence for trophoblast dysfunction in pre-eclampsia.

35 nancies could be helpful in the diagnosis of pre-eclampsia.

36 mortality was strikingly high in women with pre-eclampsia.

37 ), PCOS, heavy menstrual bleeding (HMB), and pre-eclampsia.

38 in fetal growth restriction associated with pre-eclampsia.

39 risk factor for gestational hypertension and pre-eclampsia.

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

41 tensinogen (AGT) may have a critical role in pre-eclampsia.

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

43 nancies, particularly in FGR associated with pre-eclampsia.

44 associated with gestational hypertension and pre-eclampsia.

45 olled and assessed 1035 women with suspected pre-eclampsia.

46 ing the angiogenic imbalance observed during pre-eclampsia.

47 al origin from the placenta is a hallmark of pre-eclampsia.

48 g-term maternal and fetal risks conferred by pre-eclampsia.

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

50 reduced the time to clinical confirmation of pre-eclampsia.

51 ot show a significant reduction in recurrent pre-eclampsia.

52 r more units during an average 2 years were: pre-eclampsia, 1.78 (95% CI 1.52-2.08); gestational hype

53 ransfer was associated with a higher risk of pre-eclampsia (16 of 512 [3.1%] vs four of 401 [1.0%]; R

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

55 .4]), preterm delivery (1.8 [1.3--2.5]), and pre-eclampsia (2.0 [1.5--2.5]).

56 .9, -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

57 Ninety-five (0.99%) women developed severe pre-eclampsia, 47.6% were non-European immigrants, 16.3%

58 m and postpartum haemorrhage (70% each), and pre-eclampsia (56%).

59 cated in the hypertension that characterises pre-eclampsia, a condition where tissue oedema is also o

60 Remodeling is impaired during pre-eclampsia, a disease of pregnancy that results in ma

61 uring normal pregnancy, is down regulated in pre-eclampsia, a human pregnancy disorder associated wit

62 al artery remodelling has been implicated in pre-eclampsia, a major complication of pregnancy, for a

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

64 n the general population had a lower risk of pre-eclampsia-a common pregnancy complication related to

65 l-age (SGA) birth, gestational diabetes, and pre-eclampsia according to density of fruits and vegetab

66 in placentas from pregnancies complicated by pre-eclampsia (adjusted odds ratio (aOR) 1.46, 95% CI: 1

67 Pre-eclampsia affects 2% to 8% of all pregnancies worldw

68 Pre-eclampsia affects 3-5% of pregnancies and is traditi

69 Pre-eclampsia affects approximately 5% of pregnancies an

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

71 eterm birth, PPROM, placental abruption, and pre-eclampsia aggregate in families, which may be explai

72 A case-control study (1365 cases of pre-eclampsia and 1886 normotensive controls) was conduc

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

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

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

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

77 Participants with previous pre-eclampsia and eclampsia received 500 mg calcium or p

78 r more than a century of intensive research, pre-eclampsia and eclampsia remain an enigmatic set of c

79 thologic conditions include entities such as pre-eclampsia and eclampsia, along with conditions that

80 en 62 000 and 77 000 women die annually from pre-eclampsia and eclampsia.

81 r calcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral a

82 Pre-eclampsia and fetal growth restriction arise from di

83 associated with gestational hypoxia such as pre-eclampsia and fetal growth restriction.

84 study as a critical mechanistic link between pre-eclampsia and fetal growth restriction.

85 underpins common pregnancy disorders such as pre-eclampsia and fetal growth restriction.

86 is review is to determine the association of pre-eclampsia and future cardiovascular risk and to expl

87 pertensive disorders of pregnancy, including pre-eclampsia and gestational hypertension (GHTN).

88 eported, and we estimated the RR (95% CI) of pre-eclampsia and GHTN with log-binomial regression usin

89 to Stop Hypertension (DASH) with the risk of pre-eclampsia and GHTN.

90 ause placental structural changes leading to pre-eclampsia and impaired nutrient transport causing lo

91 mplicated in pathological conditions such as pre-eclampsia and intra-uterine growth retardation.

92 re of the feto-maternal interface results in pre-eclampsia and intrauterine growth retardation.

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

94 is impaired in women who eventually develop pre-eclampsia and it occurs before the development of th

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

96 a) and activin A (> 100 kDa) were similar in pre-eclampsia and normal pregnancy.

97 ns, and activin A in the serum of women with pre-eclampsia and of healthy matched control pregnant wo

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

99 c women to test the association of them with pre-eclampsia and quantitative traits relevant for the d

100 leased by the placenta in the development of pre-eclampsia and review novel therapeutic strategies di

101 e in the prediction of both preterm and term pre-eclampsia and SGA.

102 pregnancy and investigated associations with pre-eclampsia and small-for-gestational-age (SGA) birth,

103 r studies identify a genetic mouse model for pre-eclampsia and suggest that 2-ME may have utility as

104 diagnosis, risk factors, and pathogenesis of pre-eclampsia and the present status of its prediction,

105 The clinical presentation of pre-eclampsia and toxic effects of antiretroviral therap

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

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

108 tcome of human pregnancy (ie, development of pre-eclampsia) and that, by the time delivery becomes ne

109 o had to have terminations because of severe pre-eclampsia, and 23 spontaneously aborted (<24 weeks'

110 n from 20 women in hospital with established pre-eclampsia, and from 20 control pregnant women attend

111 cy outcomes (APOs)-including pre-term birth, pre-eclampsia, and intrauterine growth restriction-are c

112 which is a potential contributory factor for pre-eclampsia, and is associated with endothelial dysfun

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

114 th heart failure, hypertension in pregnancy, pre-eclampsia, and pre-term delivery; there were no diff

115 rriage, intrauterine growth restriction, and pre-eclampsia, and raises new possibilities for interven

116 B concentrations occurs in normal pregnancy, pre-eclampsia, and SGA pregnancies.

117 ancy may be an indicator of hypertension and pre-eclampsia, and that treatment with certain neurokini

118 related immune deficiency with a low rate of pre-eclampsia, and the restoration of this rate in women

119 Oxidative stress could play a part in pre-eclampsia, and there is some evidence to suggest tha

120 to make a diagnosis in women with suspected pre-eclampsia, and whether this approach reduced subsequ

121 bolic events (aOR: 2.4; 95% CI: 2.0 to 2.9), pre-eclampsia (aOR: 1.5; 95% CI: 1.3 to 1.7), and placen

122 t intrauterine growth restriction (IUGR) and pre-eclampsia are associated with a greater degree of tr

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

124 Women with a history of pre-eclampsia are at increased risk of future cardiovasc

125 Although algorithms to predict pre-eclampsia are promising, they have yet to become val

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

127 DPs), including gestational hypertension and pre-eclampsia, are common obstetric complications associ

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

129 a two-fold higher risk of developing severe pre-eclampsia as compared to European-born women, one-fi

130 and 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 late

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

133 mplications include gestational diabetes and pre-eclampsia, both of which are associated with long-te

134 lial dysfunction is a feature of established pre-eclampsia but whether this is a cause or consequence

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

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

137 diagnostic accuracy in women with suspected pre-eclampsia, but we remain uncertain of the effectiven

138 ere identified as being at increased risk of pre-eclampsia by abnormal two-stage uterine-artery doppl

139 lt-1 expression by decidual cells to promote pre-eclampsia by interfering with local vascular transfo

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

141 When left untreated, pre-eclampsia can be lethal, and in low-resource setting

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

143 a from the Community-Level Interventions for Pre-eclampsia (CLIP) cluster randomised controlled trial

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

145 haran Africa had an increased risk of severe pre-eclampsia compared to European-born mothers (aOR 2.5

146 In pre-eclampsia, deficient HB-EGF signalling during placen

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

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

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

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

151 However, pre-eclampsia does not develop in all women with high sF

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

153 egnancy, and one mother with SPKTx developed pre-eclampsia during both pregnancies.

154 into normotensive, gestational hypertension, pre-eclampsia, eclampsia, pre-eclampsia superimposed on

155 ) among postdelivery women with a history of pre-eclampsia/eclampsia (PEE).

156 Pre-eclampsia/eclampsia are leading causes of maternal m

157 SMOs were postpartum haemorrhage and severe pre-eclampsia/eclampsia.

158 T, previously implicated in hypertension and pre-eclampsia, exhibits a similar geographic distributio

159 In pre-eclampsia, expression of the Notch ligand JAG1 was a

160 lure of transformation has been described in pre-eclampsia, fetal growth restriction, and miscarriage

161 icated in adverse obstetric outcomes such as pre-eclampsia, fetal growth restriction, and preterm bir

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

163 410 women identified as at increased risk of pre-eclampsia from 25 hospitals.

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

165 labour; breech presentation; PROM, eclampsia/pre-eclampsia; gestation 33-36 weeks; gestation 41+ week

166 eight gain and subsequently increase risk of pre-eclampsia, gestational diabetes mellitus, hypertensi

167 Pre-eclampsia, gestational hypertension, and small-for-g

168 Women who developed pre-eclampsia had significantly lower flow-mediated dila

169 Low birthweight, pre-term birth and pre-eclampsia have been associated with maternal periodo

170 liver diseases unique to pregnancy, such as pre-eclampsia; hemolysis, elevated liver enzymes, and lo

171 urological symptoms are often diagnosed with pre-eclampsia; however, a range of other causes must als

172 known to reduce the serious consequences of pre-eclampsia; however, the effect of calcium supplement

173 However, the rate of pre-eclampsia in HIV-1-positive women on treatment did n

174 in supplementation affects the occurrence of pre-eclampsia in low-risk women and to confirm our resul

175 g antiplatelet agents, for the prevention of pre-eclampsia in pregnancy.

176 n between maternal place of birth and severe pre-eclampsia in the PreCARE cohort of pregnant women in

177 and E may be beneficial in the prevention of pre-eclampsia in women at increased risk of the disease.

178 ith vitamin C and vitamin E does not prevent pre-eclampsia in women at risk, but does increase the ra

179 n with suspected pre-eclampsia to documented pre-eclampsia in women enrolled in the trial who receive

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

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

182 We show here that key features of pre-eclampsia, including hypertension, proteinuria, glom

183 and Nigeria [7.1%]; p < 0.001), followed by pre-eclampsia (India [3.8%], Nigeria [3.0%], Pakistan [2

184 completed using data from 1,300 women in the Pre-eclampsia Integrated Estimate of RiSk (fullPIERS) da

185 ce localization on placental tissue, that in pre-eclampsia invasive cytotrophoblasts fail to properly

186 nce of curative treatment, the management of pre-eclampsia involves stabilisation of the mother and f

187 Pre-eclampsia is a common pregnancy disorder that is a m

188 Pre-eclampsia is a complication of pregnancy that is ass

189 Pre-eclampsia is a disorder of pregnancy associated with

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

191 Pre-eclampsia is a multisystem placentally mediated dise

192 Pre-eclampsia is a principal cause of maternal morbidity

193 Pre-eclampsia is a severe hypertensive disorder of pregn

194 The pregnancy disease pre-eclampsia is associated with shallow cytotrophoblast

195 Pre-eclampsia is associated with significant morbidity a

196 ension and seizures, but the only 'cure' for pre-eclampsia is delivery of the dysfunctional placenta

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

198 nificance, as the downregulation of HBEGF in pre-eclampsia is likely to be a contributing factor lead

199 trast, the prediction of term and postpartum pre-eclampsia is limited and there are no preventive tre

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

201 An effective treatment of pre-eclampsia is unavailable owing to the poor understan

202 resistance placental circulation at risk of pre-eclampsia, IUGR, or both have raised concentrations

203 receptor 1 secreted from the placenta causes pre-eclampsia-like features by antagonizing vascular end

204 2-ME ameliorates all pre-eclampsia-like features without toxicity in the Comt

205 g in female mice lacking eNOS aggravates the pre-eclampsia-like phenotype induced by increased sFlt-1

206 n catechol-O-methyltransferase (COMT) show a pre-eclampsia-like phenotype resulting from an absence o

207 S/nitric oxide exacerbates the sFlt1-related pre-eclampsia-like phenotype through activation of the e

208 is associated with adverse outcomes such as pre-eclampsia, low infant birth weight, and later-life a

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

210 cal significance): multiple birth; eclampsia/pre-eclampsia; maternal age 40-44 years; placental weigh

211 Thus, our studies indicate that pre-eclampsia may be a pregnancy-induced autoimmune dise

212 who were matched for duration of gestation (pre-eclampsia mean 29.15 [SD 3.75] weeks; controls 29.30

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

214 Variants predisposing to pre-eclampsia might be under negative evolutionary selec

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

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

217 1-39.8] 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],

218 ls at the time of disease presentation (term pre-eclampsia n=14, median 22.2 ng/mL [IQR 15.1-39.8] vs

219 with gestational hypertension (n = 496) and pre-eclampsia (n = 1804) were identified from the Intern

220 ypertension and obesity; a family history of pre-eclampsia, nulliparity or multiple pregnancies; and

221 In the intention-to-treat cohort, pre-eclampsia occurred in 24 (17%) of 142 women in the p

222 Pre-eclampsia occurred in 69 (23%) of 296 participants i

223 dividuals, particularly when associated with pre-eclampsia or acute glomerulonephritis.

224 ost recent pregnancy had been complicated by pre-eclampsia or eclampsia and who were intending to bec

225 reasons for indicated preterm births include pre-eclampsia or eclampsia, and intrauterine growth rest

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

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

228 nts are correlated with low birth weight and pre-eclampsia or high birth weight and obstructed labor,

229 e fetus and required delivery as a result of pre-eclampsia or hypertension were randomly assigned (1:

230 sation for induction of labour in women with pre-eclampsia or hypertension.

231 parity or multiple pregnancies; and previous pre-eclampsia or intrauterine fetal growth restriction.

232 Blood samples from women with pre-eclampsia or SGA were analysed from the time of dise

233 tcomes associated with maternal asthma were: pre-eclampsia (OR = 2.18; 95% CI, 1.68 to 2.83), placent

234 infertility therapies (p = 0.0004), and had pre-eclampsia (p = 0.001).

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

236 idase levels were significantly decreased in pre-eclampsia patients compared to normal pregnant women

237 Pre-eclampsia (PE) and gestational diabetes mellitus (GD

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

239 Pre-eclampsia (PE) is a leading cause of maternal and fe

240 cidence of gestational hypertension (GH) and pre-eclampsia (PE) is increasing.

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

242 calcium with gestational hypertension (GH), pre-eclampsia (PE), caesarean section (CS), preterm birt

243 Placental RAS is increased in pre-eclampsia (PE), characterised by placental dysfuncti

244 Pre-eclampsia (PE), which affects approximately 8% of fi

245 normal pregnancy and in increased amounts in pre-eclampsia (PE), which have proinflammatory and antia

246 imbalance has not been fully investigated in pre-eclampsia (PE).

247 hanisms that facilitate the emergence of the pre-eclampsia phenotype in women are still unknown.

248 r endotheliosis (a classical renal lesion of pre-eclampsia), placental abnormalities and small fetus

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

250 lice site variants that were enriched in the pre-eclampsia pools compared to reference data, and geno

251 us recent studies have shown that women with pre-eclampsia possess autoantibodies, termed AT(1)-AAs,

252 Because pre-eclampsia predisposes mothers to cardiovascular dise

253 ding increased risk of gestational diabetes, pre-eclampsia, preterm birth, instrumental and caesarean

254 the group of women who eventually developed pre-eclampsia (r=-0.8, p=0.005).

255 All pre-eclampsia-related deaths were post-partum and 50% we

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

257 ology of PPCM, and why it is associated with pre-eclampsia, remain unknown.

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

259 eterm birth, PPROM, placental abruption, and pre-eclampsia, respectively).

260 associated with 1.1% and 1.4% reductions in pre-eclampsia risk compared with lower densities, respec

261 before pregnancy to 20 weeks' gestation, the pre-eclampsia risk was 30 (21%) of 144 versus 47 (32%) o

262 re or during pregnancy (RR 1.28, 1.19-1.36), pre-eclampsia (RR 1.32, 1.20-1.45), prepregnancy materna

263 ypothesis has obvious implications regarding pre-eclampsia screening, diagnosis and therapy.

264 Pooled samples of control (n = 3) and pre-eclampsia serum (n = 3) subsequently underwent fast

265 ived no antiretroviral therapy had a rate of pre-eclampsia significantly lower (none of 61) than thos

266 ependently adjudicated severe or early-onset pre-eclampsia, small-for-gestational-age infant (birthwe

267 nta-mediated pregnancy complications (severe pre-eclampsia, small-for-gestational-age infants, and pl

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

269 Meta-analyses of low-dose aspirin to prevent pre-eclampsia suggest that the incidence of preterm birt

270 onal hypertension, pre-eclampsia, eclampsia, pre-eclampsia superimposed on chronic hypertension, and

271 and pro alpha C were significantly higher in pre-eclampsia than in control normal pregnancy (inhibin

272 hibin A, pro alpha C, and total activin A in pre-eclampsia than in control pregnancies could be helpf

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

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

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

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

277 ld be discussed with women with late preterm pre-eclampsia to allow shared decision making on timing

278 as the time from presentation with suspected pre-eclampsia to documented pre-eclampsia in women enrol

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

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

281 group, 79 vitamin group), the odds ratio for pre-eclampsia was 0.24 (0.08-0.70, p=0.002).

282 Adjusted odds ratio of pre-eclampsia was 1.21 (95%CI 1.11-1.33) for every one s

283 n was 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 sc

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

285 Pre-eclampsia was assessed by the development of protein

286 Suspected pre-eclampsia was defined as new-onset or worsening of e

287 eeks gestation) or gestational (>=20 weeks); pre-eclampsia was gestational hypertension plus proteinu

288 ublished one of the earliest descriptions of pre-eclampsia was incorrectly stated to be 1637, which i

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

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

291 The incidence of pre-eclampsia was similar in treatment placebo groups (1

292 of HDPs, either gestational hypertension or pre-eclampsia, was associated with an increased risk of

293 ariants in individuals with hypertension and pre-eclampsia were defective in PCSK6-mediated activatio

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

295 Women experiencing severe pre-eclampsia were more likely to be from Sub-Saharan Af

296 ccurred in both fetal growth restriction and pre-eclampsia, whereas CD79alpha(+) B-cell infiltration

297 tect sub-Saharan Africans and Europeans from pre-eclampsia, whereas in both populations, the KIR AA g

298 reased risks of gestational hypertension and pre-eclampsia, whereas normalizing BMI from childhood to

299 The primary endpoint was pre-eclampsia, which we defined as gestational hypertens

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