Familial Aggregation of Severe Preeclampsia

Abstract: It has been proved from several studies that the genetic influence has been the most significant factor for having preeclampsia (PE). Still there are many uncertainties about origin and magnitude of the genetic effects as no specific inheritance patterns have been established. In this study, heritage risk of PE is in both the woman’s family and her partner’s family to her risk of PE is examined, along women and men own history with same and different partners. Moreover it is also examined whether timing of onset of PE is also has any impact on familial clustering of PE. Here, we used the population based Danish birth and multi generation registers to identify a cohort of women who have given birth during 1978 to 2008; which consisted of 1,79,69,28 singleton deliveries. This information is linked with pedigree information from the Danish Family Relation Database to define both maternal and paternal relationships. Risk ratios were estimated comparing women with and without various PE histories. It is found that the recurrence risk of a woman suffering from PE is 12.4 with 95% confidence limits (11.9, 12.8). Woman's recurrence risk diminishes only slightly when she changes partner means that particularly maternal genetic factors play the largest role, compared to male partner whose recurrence risk almost diminishes if he changes his female partner. Women and men from families with PE contribute to risk of PE in pregnancies they are involved in. The woman’s family history is still more important compared to man family history of PE; except for increased rick in pregnancies fathered by men who were born to preeclamptic mothers.  The recurrence risk of a women suffering from PE, if she already has suffered from this condition before 34 weeks is found to be very high (RR=25.4 with 95% confidence limits (21.8, 29.1)) with same male partner. It is found that early-onset PE and later-onset varieties have a clear genetic component but the intensity of early onset is stronger than late onset varieties. There are both maternal and paternal genetic contributions to early-onset PE, with the maternal ones seeming to be stronger.