Nilsson Emma, Salonen Ros Helena, Cnattingius Sven, Lichtenstein Paul
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
BJOG. 2004 Mar;111(3):200-6. doi: 10.1111/j.1471-0528.2004.00042x.x.
To determine the importance of genetic effects in the aetiology of pre-eclampsia and gestational hypertension and to investigate whether pre-eclampsia and gestational hypertension share genetic aetiology.
Individual record linkage between the population-based Swedish Multi-Generation and the Medical Birth Registers.
Sweden.
1,188,207 births between 1987 and 1997 and their parents.
Similarities in relatives were measured by the number of pairs concordant and discordant for disease, the odds ratio (OR) and tetrachoric correlations. Estimates of genetic and environmental effect for gestational hypertension, pre-eclampsia and pregnancy-induced hypertension were calculated from structural equation model fitting.
Pre-eclampsia and gestational hypertension.
Full sisters and mother-daughters were more similar for pre-eclampsia (OR 3.3, 95% confidence interval [CI] 3.0-3.6 and OR 2.6, 95% CI 1.6-4.3, respectively) than half-sisters (maternal half-sisters OR 1.4, 95% CI 0.9-2.2 and paternal half-sisters OR 1.0, 95% CI 0.6-1.6). Full sisters and mother-daughters were also more similar for gestational hypertension than half-sisters. A full sister to a woman with pre-eclampsia also had a significantly increased risk of gestational hypertension (OR 2.5, 95% CI 2.2-2.8). In contrast, the risk for half-sisters was not increased. Model fitting suggested heritability estimates for pre-eclampsia of 31%, for gestational hypertension 20% and for pregnancy-induced hypertension 28%.
There is a genetic component in the development of pre-eclampsia and gestational hypertension and the pattern of co-morbidity suggests that they may share part of their genetic aetiology. This could be important for studies of potential susceptibility genes for these diseases.
确定遗传效应在子痫前期和妊娠期高血压病因中的重要性,并调查子痫前期和妊娠期高血压是否具有共同的遗传病因。
基于人群的瑞典多代登记册与医疗出生登记册之间的个体记录链接。
瑞典。
1987年至1997年间的1188207例分娩及其父母。
通过疾病一致和不一致的对数、优势比(OR)和四分相关系数来衡量亲属之间的相似性。从结构方程模型拟合中计算妊娠期高血压、子痫前期和妊娠诱发高血压的遗传和环境效应估计值。
子痫前期和妊娠期高血压。
对于子痫前期,亲姐妹和母女对子痫前期的相似性(OR分别为3.3,95%置信区间[CI]3.0 - 3.6和OR 2.6,95% CI 1.6 - 4.3)高于同父异母或同母异父姐妹(母系同父异母姐妹OR 1.4,95% CI 0.9 - 2.2;父系同父异母姐妹OR 1.0,95% CI 0.6 - 1.6)。亲姐妹和母女对妊娠期高血压的相似性也高于同父异母或同母异父姐妹。子痫前期女性的亲姐妹患妊娠期高血压的风险也显著增加(OR 2.5,95% CI 2.2 - 2.8)。相比之下,同父异母或同母异父姐妹的风险没有增加。模型拟合表明,子痫前期的遗传度估计为31%,妊娠期高血压为20%,妊娠诱发高血压为28%。
子痫前期和妊娠期高血压的发生存在遗传成分,共病模式表明它们可能共享部分遗传病因。这对于这些疾病潜在易感基因的研究可能很重要。