title: Association of angiotensin-converting enzyme intron 16 insertion/deletion polymorphism with history of foetal loss.
abstract: BACKGROUND
  The angiotensin-converting enzyme (ACE) intron 16 insertion/deletion (I/D) polymorphism is associated with ACE activity and has been discussed as a risk factor for pre-eclampsia. Disturbances of uteroplacental circulation are involved in the pathogenesis of pre-eclampsia. In this study, we tested whether the ACE I/D genotype is associated with history of foetal loss (FL) or uteroplacental dysfunction (UPD).
  
  
  METHODS
  ACE I/D genotype was determined in 312 women presenting with a history of FL and 112 women admitted because of UPD. The association of the ACE I/D genotype with FL or UPD was assessed in a case-control study using 527 patients with diagnoses other than FL or UPD. To exclude potential biases due to associations of this genotype with other diagnoses, we additionally performed a case-control study using 553 healthy controls.
  
  
  RESULTS
  ACE I/D genotype was significantly associated with history of FL in both case-control studies (patient controls: odds ratio 1.52, p<0.02; healthy controls: odds ratio 1.48, p=0.02). There was no evidence for allele-dose dependency. No association of the ACE I/D genotype with UPD could be detected.
  
  
  CONCLUSIONS
  The ACE I/D genotype exhibits a statistically significant association with a history of FL. These results corroborate an involvement of the renin-angiotensin system in pregnancy complications.
authors.affiliation: Institute of Transfusion Medicine, Charité - Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany.
authors.forename: Larisa
authors.initials: L
authors.lastname: Bukreeva
authors.forename: Alexander
authors.initials: A
authors.lastname: Grigorov
authors.forename: Holger
authors.initials: H
authors.lastname: Kiesewetter
authors.forename: Berthold
authors.initials: B
authors.lastname: Hoppe
mesh_terms: D000026:Abortion, Habitual / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics / Q000503:physiopathology; D005838:Genotype; D006801:Humans; D007438:Introns; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011247:Pregnancy
chemical_list: D007703:Peptidyl-Dipeptidase A