ライフサイエンスコーパス: eclampsia

1 00 women die annually from pre-eclampsia and eclampsia.

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

3 edema-the clinical signs of preeclampsia and eclampsia.

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

5 significantly lower in women with severe pre-eclampsia.

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

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

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

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

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

11 acutely and excessively elevated, as during eclampsia.

12 ede and contribute to the development of pre-eclampsia.

13 r, small for gestational age infants, or pre-eclampsia.

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

15 plasma extravasation in diseases such as pre-eclampsia.

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

17 ed in pregnancy-induced hypertension and pre-eclampsia.

18 play a role in the etiology of preeclampsia/eclampsia.

19 ntal insufficiency and the occurrence of pre-eclampsia.

20 een implicated in the pathophysiology of pre-eclampsia.

21 f circulating inhibin A and activin A in pre-eclampsia.

22 evidence for trophoblast dysfunction in pre-eclampsia.

23 ies could be helpful in the diagnosis of pre-eclampsia.

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

25 entified in people with hypertension and pre-eclampsia.

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

27 of cytotoxic drugs, autoimmune disorders, or eclampsia.

28 he risks of gestational hypertension and pre-eclampsia.

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

30 ntitis was significantly associated with pre-eclampsia.

31 is accentuated by multiple gestation and pre-eclampsia.

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

33 mic angiogenic imbalance, accentuated by pre-eclampsia.

34 sure and proteinuria, characteristics of pre-eclampsia.

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

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

37 54 (95% CI, 1.39-1.70) after preeclampsia or eclampsia, 1.51 (95% CI, 1.27-1.80) after GH vs no HDP,

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

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

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

41 d in the hypertension that characterises pre-eclampsia, a condition where tissue oedema is also obser

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

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

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

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

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

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

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

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

50 s include entities such as pre-eclampsia and eclampsia, along with conditions that are seen with incr

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

52 re than a century of intensive research, pre-eclampsia and eclampsia remain an enigmatic set of condi

53 ogic conditions include entities such as pre-eclampsia and eclampsia, along with conditions that are

54 2 000 and 77 000 women die annually from pre-eclampsia and eclampsia.

55 lcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral antic

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

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

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

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

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

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

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

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

64 Twenty-eight patients with preeclampsia-eclampsia and neurologic symptoms underwent magnetic res

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

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

67 who received less prenatal care (OR=4.2 for eclampsia and OR=3.1 for severe preeclampsia, p<0.05 for

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

69 0.05 for both) and among Black women (OR for eclampsia and preeclampsia together=3.9, p<0.05).

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

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

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

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

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

75 The clinical presentation of pre-eclampsia and toxic effects of antiretroviral therapy co

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

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

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

79 e of human pregnancy (ie, development of pre-eclampsia) and that, by the time delivery becomes necess

80 d to have terminations because of severe pre-eclampsia, and 23 spontaneously aborted (<24 weeks' gest

81 was receiving interferon for melanoma, 3 had eclampsia, and 4 had acute hypertensive encephalopathy a

82 om 20 women in hospital with established pre-eclampsia, and from 20 control pregnant women attending

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

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

85 h is a potential contributory factor for pre-eclampsia, and is associated with endothelial dysfunctio

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

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

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

89 ge, intrauterine growth restriction, and pre-eclampsia, and raises new possibilities for intervention

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

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

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

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

94 may be an indicator of hypertension and pre-eclampsia, and that treatment with certain neurokinin re

95 ted immune deficiency with a low rate of pre-eclampsia, and the restoration of this rate in women tre

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

97 antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral anticonvulsants for

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

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

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

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

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

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

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

105 imary outcome measure was the development of eclampsia, as defined by a witnessed tonic-clonic seizur

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

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

108 anging paternity on the risk of preeclampsia/eclampsia between women with and those without a history

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

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

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

112 identified as being at increased risk of pre-eclampsia by abnormal two-stage uterine-artery doppler a

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

114 Magnesium sulfate may prevent eclampsia by reducing cerebral vasoconstriction and isch

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

116 In pre-eclampsia, deficient HB-EGF signalling during placental

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

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

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

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

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

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

123 of transformation has been described in pre-eclampsia, fetal growth restriction, and miscarriage.

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

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

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

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

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

129 Women who developed pre-eclampsia had significantly lower flow-mediated dilation

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

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

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

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

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

135 However, the rate of pre-eclampsia in HIV-1-positive women on treatment did not d

136 upplementation affects the occurrence of pre-eclampsia in low-risk women and to confirm our results i

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

138 Among women without preeclampsia/eclampsia in the first birth, changing partners resulted

139 he other hand, among women with preeclampsia/eclampsia in the first birth, changing partners resulted

140 a 30% reduction in the risk of preeclampsia/eclampsia in the subsequent pregnancy (95% confidence in

141 aternity affects the risk of preeclampsia or eclampsia in the subsequent pregnancy and whether the ef

142 n a 30% increase in the risk of preeclampsia/eclampsia in the subsequent pregnancy compared with thos

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

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

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

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

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

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

149 ocalization on placental tissue, that in pre-eclampsia invasive cytotrophoblasts fail to properly mod

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

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

152 Pre-eclampsia is a disorder of pregnancy associated with poo

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

154 Pre-eclampsia is a multisystem placentally mediated disease,

155 Pre-eclampsia is a principal cause of maternal morbidity and

156 The pregnancy disease pre-eclampsia is associated with shallow cytotrophoblast inv

157 Pre-eclampsia is associated with significant morbidity and m

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

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

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

161 istance placental circulation at risk of pre-eclampsia, IUGR, or both have raised concentrations of A

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

163 2-ME ameliorates all pre-eclampsia-like features without toxicity in the Comt(-/-

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

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

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

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

168 were matched for duration of gestation (pre-eclampsia mean 29.15 [SD 3.75] weeks; controls 29.30 [3.

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

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

171 .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

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

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

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

175 duals, particularly when associated with pre-eclampsia or acute glomerulonephritis.

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

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

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

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

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

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

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

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

184 es associated with maternal asthma were: pre-eclampsia (OR = 2.18; 95% CI, 1.68 to 2.83), placenta pr

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

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

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

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

189 Pre-eclampsia (PE) is a leading cause of maternal and fetal

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

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

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

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

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

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

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

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

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

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

200 Because pre-eclampsia predisposes mothers to cardiovascular disease

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

202 This rare syndrome frequently is seen with eclampsia/preeclampsia and is associated with high mater

203 after experiencing an atypical preeclampsia-eclampsia presentation known today as the HELLP syndrome

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

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

206 ury of intensive research, pre-eclampsia and eclampsia remain an enigmatic set of conditions.

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

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

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

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

211 usted relative risks (RRs) = 4.89 and 2.01), eclampsia (RRs = 3.58 and 1.67), anemia (RRs = 2.23 and

212 ronic hypertension (RRs = 4.66 and 3.15) and eclampsia (RRs = 6.28 and 5.08).

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

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

215 no antiretroviral therapy had a rate of pre-eclampsia significantly lower (none of 61) than those on

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

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

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

219 pro alpha C were significantly higher in pre-eclampsia than in control normal pregnancy (inhibin A 3.

220 n A, pro alpha C, and total activin A in pre-eclampsia than in control pregnancies could be helpful i

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

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

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

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

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

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

227 Pre-eclampsia was assessed by the development of proteinuric

228 at MR imaging in patients with preeclampsia-eclampsia was associated with abnormalities in endotheli

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

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

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

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

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

234 depends on a woman's history of preeclampsia/eclampsia with her previous partner, a cohort study was

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

236 rnity depends on the history of preeclampsia/eclampsia with the previous partner and support the hypo