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Genetic and familial predisposition to eclampsia and pre‐eclampsia in a defined population
Author(s) -
ARNGRIMSSON REYNIR,
BJÖRNSSON STEINGRIMUR,
GEIRSSON REYNIR T.,
BJÖRNSSON HÓLMGEIR,
WALKER JAMES J.,
SNAEDAL GUNNLAUGUR
Publication year - 1990
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/j.1471-0528.1990.tb02569.x
Subject(s) - penetrance , eclampsia , daughter , population , inheritance (genetic algorithm) , family aggregation , preeclampsia , genetics , genetic model , demography , medicine , pregnancy , biology , gene , evolutionary biology , phenotype , sociology
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.