Polymorphisms of the angiotensin converting enzyme gene in early-onset and late-onset pre-eclampsia.

The aim of this study was to investigate differences in maternal and infant ACE genotypes in early-onset and later-onset pre-eclampsia/toxemia (PET). We conducted a case-control study of 22 cases of early-onset pre-eclampsia (before 34 weeks gestation), 38 cases of later-onset pre-eclampsia (after 34 weeks gestation), and 108 healthy controls delivered at term (38-40 weeks gestation) within a stable Caucasian population. Maternal venous blood and cord bloods were obtained for serum angiotensin converting enzyme (ACE) activity, ACE genotype, and acid-base status. Mothers who developed early-onset PET were more likely to be homozygous for the deletion allele of the ACE genotype (DD) than mothers with late-onset PET or uncomplicated pregnancies (12/22 (55%) vs. 7/38 (18%) vs. 22/105 (21%), respectively; OR 2.96 [95% confidence intervals (CI) 1.37-6.31]. Infants of mothers with early-onset PET were more likely to be homozygous for the DD genotype than infants of mothers with late-onset PET or controls (7/19 (37%) vs. 9/36 (25%) vs. 11/78 (14%); OR 2.51 (95% CI 1.12-5.61). There were no differences in maternal or infant ACE activities in relation to onset of pre-eclampsia. Our findings suggest an association between the DD genotype of the ACE gene and early-onset but not later-onset pre-eclampsia which may give a partial explanation for the higher recurrence risk with early-onset pre-eclampsia.