Association between Estrogen Receptor .ALPHA. (ESR1) Gene Polymorphisms and Severe Preeclampsia

Molvarec, Attila; Vér, Ágota; Fekete, Andrea; Rosta, Klára; Derzbach, László; Derzsy, Zoltán; Karádi, István; Rigó, János

doi:10.1291/hypres.30.205

Cited by 64 publications

(46 citation statements)

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“…40 Nevertheless, the serum and urine levels of this protein did not correlate in patients with various renal diseases. 41 In preeclampsia, decreased estrogen levels and action have been observed in previous studies, 10,42 which might also result in lower AHSG concentrations. Moreover, the role of AHSG gene polymorphisms has not been investigated yet in this pregnancy-specific disorder.…”

Section: Discussionmentioning

confidence: 73%

“…[5][6][7][8] The development of preeclampsia is influenced by both genetic and environmental risk factors, suggesting its multifactorial inheritance. [9][10][11][12][13][14] The a 2 -Heremans-Schmid (a 2 -HS) glycoprotein (fetuin-A, AHSG), the human homolog of bovine fetuin, is an abundant plasma/serum protein synthesized predominantly by hepatocytes. 15 It belongs to the cystatin superfamily of cysteine proteinase inhibitors.…”

Section: Introductionmentioning

confidence: 99%

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Preeclampsia is associated with decreased serum α2-HS glycoprotein (fetuin-A) concentration

et al. 2009

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The purpose of this study was to determine serum a 2 -HS glycoprotein (AHSG) concentration and its diagnostic accuracy in preeclampsia. In this case-control study, the serum C-reactive protein (CRP) and AHSG levels were measured in 93 preeclamptic patients and in 127 healthy pregnant women by immunoturbidimetry and radial immunodiffusion. The serum CRP levels were significantly higher, whereas the serum AHSG concentrations were significantly lower in the preeclamptic group than in the control group (median (25th to 75th percentile), CRP: 6.71 mg l À1 (2.76-12.69) vs. 3.38 mg l À1 (1.69-7.27), respectively; AHSG: 660 lg ml À1 (612-768) vs. 744 lg ml À1 (660-816), respectively; Po0.001 for both). In preeclamptic patients, the serum AHSG concentrations showed significant inverse correlations with systolic blood pressure and serum CRP levels. A low serum AHSG level (p720 lg ml À1 ) was significantly associated with preeclampsia (adjusted odds ratio (95% confidence interval): 3.69 (1.82-7.51); Po0.001). According to the receiver operating characteristic curves, the measurement of serum AHSG concentrations was as accurate as that of serum CRP levels to detect preeclampsia. In conclusion, serum AHSG concentration is decreased and reflects-at least partly-systemic inflammation in preeclampsia.

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Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Preeclampsia is associated with decreased serum α2-HS glycoprotein (fetuin-A) concentration

et al. 2009

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“…Considering that cytokine gene polymorphism may influence disease susceptibility, severity and outcome, 7,19,20 our purpose was to investigate whether polymorphisms in genes, TNF-a promoter (À308 G4A), IL6 promoter (À174 G4C), IFN-g intron 1 (+874 A4T), IL10 promoters (À1082 A4G), (À819 C4T) and (À592 C4A) and TGF-b1 codon 10 (+869 T4C) and codon 25 (+915 G4C) are associated with E and/or PE in a northeastern Brazilian population.…”

Section: Introductionmentioning

confidence: 99%

Cytokine gene polymorphisms in preeclampsia and eclampsia

Lima¹,

Sass

Mattar

et al. 2009

Hypertens Res

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The clinical spectrum of preeclampsia (PE) ranges from mild hypertension to severe vasospasm associated with convulsions and multiple organ damage. The biological factors that determine the progression of PE to eclampsia (E) are unknown. Endothelial cell activation seems related to an impaired maternal immune response. The production of cytokines, IL-10 and TGF-b1, is apparently suppressed, and altered IL-2/IL-10 and TNF-a/IL-10 ratios have been reported in preeclamptic cases. The relationship between PE and cytokine gene polymorphism has been studied, but there are few studies that include eclamptic patients. This study aimed at investigating whether polymorphisms in genes, TNF-a promoter (À308 G4A), IL6 promoter (À174 G4C), IFN-c intron 1 (+874 A4T), IL10 promoters (À1082 A4G), (À819 C4T) and (À592 C4A) and TGF-b1 codon 10 (+869 T4C) and codon 25 (+915 G4C) are associated with E and/or PE. Genotyping was carried out in 266 Mulatto women from the northeastern region of Brazil who were referred to a single maternity hospital: 92 with PE, 73 with E and 101 normotensive controls. The v 2 or Fisher's exact tests were used to compare genotype frequencies. Among the six singlenucleotide polymorphisms (SNPs) studied, we found no difference in genotype frequencies between the groups. There was a higher frequency of IFN-c (+874 A) in eclamptic patients in comparison with that in controls. (70.3 vs. 57.8%, respectively; P¼0.02). There were no other significant differences in allelic frequencies between eclamptic, preeclamptic and control groups We found no independent association between any single SNP and PE or E risk in this population of Mulatto women from the northeastern region of Brazil.

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“…Several studies of polymorphisms of estrogen receptor gene also suggested the possible implication of estrogen for the genesis of PE. [31][32][33][34] Molvarec et al 34 speculated that the reduced estrogen receptor alpha (ESR1) expression in pregnant women associated with certain ESR1 gene polymorphisms might disturb the ESR1-mediated effects of estrogen, leading to a relative estrogen-deficient state. Estrogen has several effects on vascular tissues and systemic effects, such as vasodilatory effects, acceleration of re-endothelialization after vascular injury, inhibition of the vascular injury response, changes in lipid profiles, alterations in coagulation and fibrinolytic systems and antioxidant effects; therefore, the relative estrogen deficit might lead to vasoconstriction in the systemic and uteroplacental circulation in pregnant women and may influence the risks of PE.…”

Section: Discussionmentioning

confidence: 99%

Plasma level of hydroxysteroid (17-β) dehydrogenase 1 in the second trimester is an independent risk factor for predicting preeclampsia after adjusting for the effects of mean blood pressure, bilateral notching and plasma level of soluble fms-like tyrosine kinase 1/placental growth factor ratio

et al. 2012

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Mean blood pressure (MBP), bilateral notching (BN) in the uterine artery and increased circulating levels of soluble fms-like tyrosine kinase-1/placental growth factor (sFlt-1/PlGF) ratio are predictors of preeclampsia (PE). Recently, we disclosed that reducing the plasma level of hydroxysteroid (17-b) dehydrogenase 1 (HSD17B1), which is a steroidogenetic enzyme catalyzing the conversion of estrone to 17b-estradiol, is a potential prognostic factor for PE. Our aim was to evaluate whether HSD17B1 is an independent risk factor for predicting PE after adjusting for the effects of MBP, BN and the plasma level of the sFlt-1/PlGF ratio in the second trimester. One hundred and twenty-eight consecutive normal pregnant women without gestational hypertension (GH) or PE and 30 women with PE were selected from 1724 pregnant women. Multivariate logistic regression with a forward stepwise procedure was used to construct a prediction model. A past history of GH/PE, a family history of hypertension, pre-pregnancy body mass index, MBP, BN, plasma levels of sFlt-1/PlGF ratio and plasma levels of HSD17B1 were significantly associated with the occurrence of PE; however, only MBP (OR (95% confidence interval), 1.08 (1.03-1.14)), BN (7.5 (1.9-30)), sFlt-1/PlGF (21 (2.7-163)) and HSD17B1 (0.43 (0.22-0.85)) were independent risk factors for PE. The area under the receiver-operating-characteristic curve for the combination model was 0.89, yielding a sensitivity of 0.84, a specificity of 0.88 and a positive likelihood ratio of 7.2 (4.0-13). In conclusion, HSD17B1 is an independent risk factor for PE, and the combination of several risk factors including HSD17B1 in the second trimester may improve the prediction of PE.

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Association between Estrogen Receptor .ALPHA. (ESR1) Gene Polymorphisms and Severe Preeclampsia

Cited by 64 publications

References 38 publications

Preeclampsia is associated with decreased serum α2-HS glycoprotein (fetuin-A) concentration

Preeclampsia is associated with decreased serum α2-HS glycoprotein (fetuin-A) concentration

Cytokine gene polymorphisms in preeclampsia and eclampsia

Plasma level of hydroxysteroid (17-β) dehydrogenase 1 in the second trimester is an independent risk factor for predicting preeclampsia after adjusting for the effects of mean blood pressure, bilateral notching and plasma level of soluble fms-like tyrosine kinase 1/placental growth factor ratio

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