Concordance for pre‐eclampsia in monozygous twins

Lachmeijer, A. M. A.; Aarnoudse, Jg; Kate, Leo P. ten; Pals, Gerard; Dekker, Gustaaf A.

doi:10.1111/j.1471-0528.1998.tb10012.x

Cited by 17 publications

(16 citation statements)

References 5 publications

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“…However, most of the recent data rule out simple genetic mechanisms such as a single acting dominant gene (2,4,(22)(23)(24). Some studies have implicated two genes as risk factors for pre-eclampsia, AGT (encoding angiotensinogen, a precursor of the vasoconstrictor angiotensin) (25) and NOS3 (encoding endothelial nitric oxide synthestase, eNOS) (26), but the findings have not been universally confirmed (2,4). It is important to note that the AGT and NOS3 genes are also risk factors for hypertension.…”

Section: Current Genetic and Pathophysiological Models Of Pre-eclampsiamentioning

confidence: 99%

“…In addition, pre-existing essential hypertension increases the risk of pre-eclampsia (27,28). Different genome-wide scans have usually implicated more than one locus, and across all the studies loci have been identified on chromosomes 1, 2p13, 2q, 3p, 4q, 9, 10q, 11q23-24, 12q, 15q, 18 and 22q (4). Based on these data, it has been suggested that pre-eclampsia may be a multigenic disease (2,4).…”

Section: Current Genetic and Pathophysiological Models Of Pre-eclampsiamentioning

confidence: 99%

“…The requirement for a fetal-maternal interaction has lead to speculation that development of pre-eclampsia may require both feto-placental defects as well as maternal susceptibility to hypertensive and renal disease (1)(2)(3)(4). If this model were correct, it would demand very complex analysis of maternal, paternal and fetal DNA in order to identify the genetic basis of pre-eclampsia.…”

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confidence: 99%

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The genetics of pre‐eclampsia: a feto‐placental or maternal problem?

Cross

2003

Clinical Genetics

128

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Pre-eclampsia is a potentially life-threatening disease of women during pregnancy leading to hypertension and proteinuria. It affects 1 in 15 pregnancies but, despite intense research efforts, the cause of the disease remains mysterious. Because pre-eclampsia only occurs during pregnancy and its symptoms resolve after delivery, factors from the placenta are thought to be involved. The role of the placenta could be production of 'abnormal' factors that initiate widespread inflammation and vaso-constriction. Alternatively, because the placenta normally contributes to maternal cardiovascular adaptations of pregnancy, it may be that normal placental functions fail in pre-eclampsia or that susceptibilities in the mother to hypertensive, vascular and/or renal disease prevent the appropriate normal responses to them. The potential contributions of both maternal and fetal genes to the onset of the disease have complicated the genetic analysis of the disease in humans. Recent studies have identified strains of transgenic and mutant mice that develop the hallmark features of pre-eclampsia-like disease - gestational hypertension, proteinuria and kidney lesions (glomerulosclerosis). Comparison of three different mouse models suggests that pre-eclampsia can be initiated by at least three independent mechanisms: pre-existing borderline maternal hypertension that is exacerbated by pregnancy (BPH/5 strain of mice), elevated levels of the vasoconstrictor angiotensin II in the maternal circulation by placental over-production of renin (renin/angiotensinogen transgenic mice), and placental pathology (p57Kip2 mutant mice). These findings imply that the pathogenesis of pre-eclampsia cannot be explained by a single mechanism. Therefore, segregation of the human disease into different subtypes may be a key first step in identifying genetic risk factors.

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Section: Current Genetic and Pathophysiological Models Of Pre-eclampsiamentioning

confidence: 99%

Section: Current Genetic and Pathophysiological Models Of Pre-eclampsiamentioning

confidence: 99%

mentioning

confidence: 99%

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The genetics of pre‐eclampsia: a feto‐placental or maternal problem?

Cross

2003

Clinical Genetics

128

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“…There are suggestions that the fetal genome may be at least partly responsible for the development of pre‐eclampsia. Small case series suggest concordance for pre‐eclampsia in identical twins 27,28 , but a large cohort study found no evidence of concordance 29 . Changing paternity, and thus changing maternal–paternal genomic expression in the fetus, is associated with an increased risk of pre‐eclampsia 12 .…”

Section: Risk Of Bias In the Selection Of Normal Pregnancy Controlsmentioning

confidence: 99%

Is there an increased maternal–infant prevalence of Factor V Leiden in association with severe pre‐eclampsia?

Currie

Peek

McNiven

et al. 2002

BJOG

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Objective To compare the prevalence of the Factor V Leiden mutation in children and maternal–infant pairs in pregnancies affected by severe pre‐eclampsia with unmatched normal controls. Design Prospective cohort study. Setting Department of Women's and Children's Health, The Canberra Hospital, Garran, ACT, Australia. Sample Forty‐eight maternal–infant pairs where the index pregnancy was affected by severe pre‐eclampsia; 46 unmatched maternal–infant pairs where the index pregnancy was defined as normal. Methods DNA analysis of cheek swab samples obtained from maternal–infant pairs for the Factor V Leiden mutation. Main outcome measure The prevalence of the Factor V Leiden mutation in mothers, infants and maternal–infant pairs in association with severe pre‐eclampsia compared with unmatched controls. Results No difference was detected in the prevalence of Factor V Leiden mutation between the women and children of both groups, nor the maternal–infant pairs from each group. Conclusions No evidence was found of an increased prevalence of the Factor V Leiden mutation in either the mothers or children in association with severe pre‐eclampsia. This result argues against a Factor V Leiden fetal or maternal contribution to the development of severe pre‐eclampsia.

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“…There have been two reports of concordance in monozygotic twins identified when recruiting affected family members for genetic studies [7,8] and a study of 917 monozygotic and 1199 dizygotic twins using the Swedish Twin Register and Swedish Medical Birth Register predicted a heritability of 0.54 (95% confidence interval 0-0.71) [9]. However, two studies have not found concordance in monozygotic twins [10,11].…”

Section: Introductionmentioning

confidence: 92%

Molecular biology related to pre-eclampsia

Williamson

2005

International Congress Series

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Concordance for pre‐eclampsia in monozygous twins

Cited by 17 publications

References 5 publications

The genetics of pre‐eclampsia: a feto‐placental or maternal problem?

The genetics of pre‐eclampsia: a feto‐placental or maternal problem?

Is there an increased maternal–infant prevalence of Factor V Leiden in association with severe pre‐eclampsia?

Molecular biology related to pre-eclampsia

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