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Journal of Renin-Angiotensin-Aldosterone System
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Article

Association of angiotensin-converting enzyme intron 16 insertion/deletion polymorphism with history of foetal loss

Larisa Bukreeva1, Alexander Grigorov1, Holger Kiesewetter1, and Berthold Hoppe, Dr.2*

1 Institute of Transfusion Medicine, Charité – Universitätsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany
2 Central Institute of Laboratory Medicine and Pathobiochemistry, Charité – Universitätsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany

* To whom correspondence should be addressed. E-mail: berthold.hoppe{at}charite.de.


   Abstract

Introduction. 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).

Patients and 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.

First published on August 28, 2009
Journal of Renin-Angiotensin-Aldosterone System 2009, doi:10.1177/1470320309343813


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