Fetal and maternal contributions to risk of pre-eclampsia: population based study

Lie, Rolv Terje; Rasmussen, Svein; Brunborg, Helge; Gjessing, Håkon K.; Lie-Nielsen, Erik; Irgens, Lorentz M.

doi:10.1136/bmj.316.7141.1343

Cited by 424 publications

(303 citation statements)

References 20 publications

(19 reference statements)

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“…Deliveries (12 804) took place during the study period. The Norwegian Medical Birth Registry records information on all deliveries that take place in the country (Lie et al, 1998), and we used this information to identify cases of pre-eclampsia and to select appropriate controls, as previously described (Ødegård et al, 2000).…”

Section: Methodsmentioning

confidence: 99%

Alpha-foetoprotein in umbilical cord in relation to severe pre-eclampsia, birth weight and future breast cancer risk

et al. 2002

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Women born after pre-eclamptic pregnancies have been reported to be at reduced risk of breast cancer as adults, because of reduced intrauterine oestrogen influence on breast tissue; high levels of a-foetoprotein (a glycoprotein with anti-oestrogenic properties), however, could also be important. In severe pre-eclampsia, placental function and foetal growth are reduced, and umbilical cord plasma levels of a-foetoprotein could reflect the underlying processes. Umbilical cord blood was collected in 12 804 consecutive deliveries. Among 307 pregnancies with clinical pre-eclampsia, 66 singleton pregnancies were identified as clinically severe, and 610 singleton pregnancies were selected as controls. Oestradiol and a-foetoprotein were measured from umbilical plasma, and birth weight was standardized as the ratio between the observed and expected birth weight, adjusted for differences in gestation length and offspring sex. Cord plasma levels of a-foetoprotein were significantly higher in severe pre-eclampsia than controls (P50.01) after adjustment for gestational age and birth weight. For oestradiol, there was no difference in cord plasma levels between the severe pre-eclampsia group and controls, after adjustment for length of gestation and birth weight. These results suggest that an anti-oestrogenic effect associated with pre-eclampsia may be mediated through high levels of a-foetoprotein rather than low levels of oestradiol.

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Section: Methodsmentioning

confidence: 99%

Alpha-foetoprotein in umbilical cord in relation to severe pre-eclampsia, birth weight and future breast cancer risk

et al. 2002

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“…Affected mothers might carry susceptibility genes, but can also transmit independent genetic risk factors to their fetus, whereas affected fathers transmit only triggering fetal risk factors (Skjaerven et al, 2005). Men who fathered a pre-eclamptic pregnancy in one woman are more likely to father a pre-eclamptic pregnancy in other women (Lie et al, 1998). Another finding supporting the hypothesis of paternal contribution to pre-eclampsia is that long-term sperm exposure with the same partner is protective, although the risk increases in couples recently married or those who have limited sperm exposure to the same partner before conception (including barrier conception and artificial insemination) (Trupin et al, 1996;Li and Wi, 2000;Wang et al, 2002;Einarsson et al, 2003).…”

Section: Pre-eclampsiamentioning

confidence: 99%

Paternal age and reproduction

Sartorius

Nieschlag

2009

Human Reproduction Update

291

212

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background: Due to various sociological factors, couples in developed countries are increasingly delaying childbearing. Besides ethical, economical and sociological issues, this trend presents us with several complex problems in reproduction. Although it is well-known that maternal age has a negative effect on fertility and increases the risk of adverse outcome during pregnancy and in offspring, the paternal influence on these outcomes is less well researched and not well-known.methods: We performed a systematic search of PubMed, and retrieved original articles and review articles to update our previous survey in this journal.results: This review highlights the link between male age and genetic abnormalities in the germ line and summarizes the knowledge about the effects of paternal age on reproductive function and outcome. Increasing paternal age can be associated with decreasing androgen levels, decreased sexual activity, alterations of testicular morphology and a deterioration of semen quality (volume, motility, morphology). Increased paternal age has an influence on DNA integrity of sperm, increases telomere length in spermatozoa and is suggested to have epigenetic effects. These changes may, at least in part, be responsible for the association of paternal age over 40 years with reduced fertility, an increase in pregnancy-associated complications and adverse outcome in the offspring. conclusion: Although higher maternal age can be an indication for intensive prenatal diagnosis, including invasive diagnostics, consideration of the available evidence suggests that paternal age itself, however, provides no rationale for invasive procedures.

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“…Role of the maternal and fetal genotype in the development of preeclampsia is a topic of heated scientific debate. [51][52][53] Here, we demonstrate that at least for TTD-associated mutations in XPD, preeclampsia is unequivocally mediated by the fetal genotype. To the best of our knowledge, the penetrance of XPD mutations with respect to preeclampsia is highest compared to mutations reported in other genes.…”

Section: Discussionmentioning

confidence: 56%

Phenotype-specific adverse effects of XPD mutations on human prenatal development implicate impairment of TFIIH-mediated functions in placenta

et al. 2012

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Mutations in XPD (ERCC2), XPB (ERCC3), and TTD-A (GTF2H5), genes involved in nucleotide excision repair and transcription, can cause several disorders including trichothiodystrophy (TTD) and xeroderma pigmentosum (XP). In this study, we tested the hypothesis that mutations in the XPD gene affect placental development in a phenotype-specific manner. To test our hypothesis and decipher potential biologic mechanisms, we compared all XPD-associated TTD (n¼43) and XP (n¼37) cases reported in the literature with respect to frequencies of gestational complications. Our genetic epidemiologic investigations of TTD and XP revealed that the exact genetic abnormality was relevant to the mechanism leading to gestational complications such as preeclampsia. Through structural mapping, we localized the preeclampsia-associated mutations to a C-terminal motif and the helicase surfaces of XPD, most likely affecting XPD's binding to cdk-activating kinase (CAK) and p44 subunits of transcription factor (TF) IIH. Our results suggested a link between TTD-but not XP-associated XPD mutations, placental maldevelopment and risk of pregnancy complications, possibly due to impairment of TFIIH-mediated functions in placenta. Our findings highlight the importance of the fetal genotype in development of gestational complications, such as preeclampsia. Therefore, future studies of genetic associations of preeclampsia and other placental vascular complications may benefit from focusing on genetic variants within the fetal DNA.

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Fetal and maternal contributions to risk of pre-eclampsia: population based study

Cited by 424 publications

References 20 publications

Alpha-foetoprotein in umbilical cord in relation to severe pre-eclampsia, birth weight and future breast cancer risk

Alpha-foetoprotein in umbilical cord in relation to severe pre-eclampsia, birth weight and future breast cancer risk

Paternal age and reproduction

Phenotype-specific adverse effects of XPD mutations on human prenatal development implicate impairment of TFIIH-mediated functions in placenta

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