Genetic and familial predisposition to eclampsia and pre-eclampsia in a defined population
Article first published online: 19 AUG 2005
DOI: 10.1111/j.1471-0528.1990.tb02569.x
Issue
1471-0528/asset/cover.gif?v=1&s=b4e1d96c46e18c61210d584b63c13ee375cf562b)
BJOG: An International Journal of Obstetrics & Gynaecology
Volume 97, Issue 9, pages 762–769, September 1990
Additional Information
How to Cite
ARNGRIMSSON, R., BJÖRNSSON, S., GEIRSSON, R. T., BJÖRNSSON, H., WALKER, J. J. and SNAEDAL, G. (1990), Genetic and familial predisposition to eclampsia and pre-eclampsia in a defined population. BJOG: An International Journal of Obstetrics & Gynaecology, 97: 762–769. doi: 10.1111/j.1471-0528.1990.tb02569.x
Publication History
- Issue published online: 19 AUG 2005
- Article first published online: 19 AUG 2005
- Received I February 1990 Accepted 24 May 1990
- Abstract
- References
- Cited By
Summary. Familial predisposition and patterns of genetic inheritance of eclampsia and pre-eclampsia were investigated through three or four generations in 94 families from the homogenous island population of Iceland. The families descended from index women delivered in the years 1931–47 and who had either eclampsia (n = 38) or severe preeclampsia (n = 69). Inheritance was followed both through sons and daughters. The prevalence of pre-eclampsia and eclampsia in daughters was significantly higher (23%) than that in daughters-in-law (10%). No difference was noted in the prevalence of these diseases by whether the daughter was born of an eclamptic or pre-eclamptic mother or whether she was a first or later born daughter. There was a non-significantly higher occurrence of pre-eclampsia among grand-daughters than in grand-daughters-in-law. No difference was seen by whether granddaughters descended through sons or daughters. With increasing numbers of affected daughters or grand-daughters the probability rose of finding more affected women in a family. Hypotheses of single recessive and dominant gene inheritance were compared and maximum likelihood estimates for gene frequency obtained. For a single recessive gene model this was 0.31 reflecting a population prevalence of 9.6%, whereas a dominant model with incomplete penetrance gave 0.14 at 48% gene penetrance, corresponding to a population prevalence of 0.9% homozygous expression of severe disease and 11% heterozygous expression of milder disease. Either genetic model could fit the data.

1471-0528/asset/BJO_left.gif?v=1&s=0fb87361cdb6be25fdf05019eed6d47f5143f610)
1471-0528/asset/olbannerright.gif?v=1&s=3892ef16ff18d6834c302faf85268a49f5fc588f)