Association Between Susceptibility to Pre-Eclampsia Within Families and Hla Dr4

Kilpatrick, D. C.; Gibson, F. M.; Liston, W.A.; Livingstone, Jean

doi:10.1016/s0140-6736(89)91079-9

Cited by 59 publications

(23 citation statements)

References 10 publications

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“…These results refute the hypothesis from segregation studies that pre‐eclampsia with proteinuria in first pregnancies is inherited in Mendelian fashion 2,17,18 as either a recessive 3,4 or dominant phenotype 5 . We believe that the present findings are more secure than these previous studies because of the care that we took to avoid bias in our case diagnoses and because segregation studies are notoriously liable to suggest, falsely, inheritance patterns compatible with a single gene 19 .…”

Section: Discussionsupporting

confidence: 61%

Twin mothers, pregnancy hypertension and pre‐eclampsia

Thornton

Macdonald

1999

BJOG

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Objective To estimate the maternal genetic contribution to the hypertensive diseases of pregnancy.Design A cohort study of female twins with information on hypertensive diseases of pregnancy obtained by questionnaire screening, and verification of diagnosis from hospital or general practitioner records.Setting A volunteer twin registry in the UK with recruitment through the media without reference to pregnancies or disease status.Population Adult female, same-sex twin pairs who completed a pregnancy history questionnaire and consented to record inspection.Main outcome measure Self-reported and hospital-validated diagnosis of non-proteinuric pregnancy hypertension and of pregnancy hypertension with proteinuria (pre-eclampsia).Results Self-reported pre-eclampsia had a heritability of 0.221 and non-proteinuric hypertension of 0.198. However, none of the pairs who were self-reported as concordant for pre-eclampsia were confirmed from hospital records. Using hospital records, the heritability of pre-eclampsia was 0 and 0.375 for non-proteinuric hypertension. Using a model treating pre-eclampsia as a separate disease from non-proteinuric hypertension, and assuming that the next pair identified was both monozygotic and concordant for pre-eclampsia, the estimated heritability of pre-eclampsia remained 0 (95% CI 0-0-49). Using a threshold model in which non-proteinuric hypertension is treated as a mild form of pre-eclampsia, heritability is estimated at 0.247 (95% CI 0.234454). ConclusionNeither non-proteinuric hypertension nor pre-eclampsia are inherited in simple Mendelian fashion. The genetic contribution to multi-factorial inheritance is smaller than hitherto believed.

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Section: Discussionsupporting

confidence: 61%

Twin mothers, pregnancy hypertension and pre‐eclampsia

Thornton

Macdonald

1999

BJOG

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“…Eight studies examined the association between couple HLA sharing and preeclampsia, with disparate findings. Some (Jenkins et al, 1978; Fujisawa, 1985; Bolis et al, 1987; Kilpatrick et al, 1989; de Luca Brunori et al, 2000; Ooki et al, 2008) found an increased risk of preeclampsia with increased HLA sharing. However, since the fetus can inherit one of two alleles from the father, it is more likely that the HLA of the fetus rather than that of the father is most important.…”

Section: Discussionmentioning

confidence: 99%

Maternal–fetal HLA sharing and preeclampsia: variation in effects by seminal fluid exposure in a case–control study of nulliparous women in Iowa

Triche

Harland

Field

et al. 2014

Journal of Reproductive Immunology

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Whereas histocompatibility is critical for transplantation, HLA histoincompatibility is associated with successful pregnancy. Literature on HLA sharing and preeclampsia has been inconsistent; most studies focused on maternal–paternal rather than maternal–fetal sharing. This study examines whether maternal–fetal histocompatibility is associated with preeclampsia, and whether effects vary by semen exposure history. This case–control study of nulliparous women was designed to examine associations among HLA sharing, semen exposure, and preeclampsia. 258 preeclampsia cases and 182 normotensive controls met the eligibility criteria. HLA typing for mother and baby was performed for HLA-A, -B, -C, -DRB1, and -DQB1. We further restricted our study sample to 224 mother–baby pairs who had complete HLA typing for all five genes. Seminal fluid exposure indexes incorporated information on type of practice, frequency, contraceptive use (for vaginal exposure) and ingestion practices (for oral exposure). Multivariate models were adjusted for BMI and education. HLA-A matching, Class I matching, and combined Class I and II matching were associated with increased odds of preeclampsia. Among women with low semen exposure, effects of Class I matching were amplified (HLA-A matching, OR=6.27, 95%CI=1.04, 37.97; Class I matching, OR=4.49 per one-match increase, 95%CI=1.89, 14.50). With moderate to high semen exposure, Class II matching effects predominated (HLA-DQB1, OR=3.22, 95%CI=1.04, 9.99; Class II, OR=1.76 per one-match increase, 95%CI=1.05, 2.98; and total matches, OR=1.45 per one-match increase, 95%CI=1.02, 2.06). We found consistent evidence that maternal–fetal HLA sharing was associated with preeclampsia in a pattern influenced by prior vaginal exposure to paternal seminal fluid.

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“…The former include maternal hypertension, renal disease, obesity, and diabetes. 1,4 The latter include such risk factors as first pregnancy, 1 presence of HLA-DR4, 5 differing paternity, 6 short parental cohabitation time, 7 and paternal family history of preeclampsia. 8 There is overlap between these two groups with risk factors such as previous preeclampsia and maternal history of autoimmune disease such as Graves' disease, Type I diabetes, and systemic lupus erythematosus.…”

Section: Discussionmentioning

confidence: 99%