Thromb Haemost 2003; 89(05): 847-852
DOI: 10.1055/s-0037-1613472
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

The deletion polymorphism in the angiotensin-converting enzyme gene is a moderate risk factor for venous thromboembolism

Mario von Depka
1   Department of Haematology/Oncology, Hannover Medical School, Hanover, Germany
,
Andreas Czwalinna
1   Department of Haematology/Oncology, Hannover Medical School, Hanover, Germany
,
Cornelia Wermes
1   Department of Haematology/Oncology, Hannover Medical School, Hanover, Germany
,
Roswith Eisert
1   Department of Haematology/Oncology, Hannover Medical School, Hanover, Germany
,
Inge Scharrer
2   Centre of Internal Medicine I, University Hospital Frankfurt, Frankfurt, Germany
,
Arnold Ganser
1   Department of Haematology/Oncology, Hannover Medical School, Hanover, Germany
,
Silke Ehrenforth
2   Centre of Internal Medicine I, University Hospital Frankfurt, Frankfurt, Germany
› Author Affiliations
Further Information

Publication History

Received after 04 September 2002

Accepted after revision 27 February 2003

Publication Date:
09 December 2017 (online)

Summary

ACE displays potent vasoconstrictive effects, attenuation of fibrinolysis, and platelet activation and aggregation, thus possibly promoting venous thromboembolism (VTE). The ACE gene contains an insertion (I) or deletion (D) polymorphism accounting for 50% of the variation in serum ACE concentration. To evaluate the role of the I/D polymorphism in VTE, its prevalence was determined in 931 patients with VTE and 432 blood donors. The prevalence of the DD genotype was 27.6% in patients and 21.3% in controls (OR 1.4; p <0.02). In multivariate analysis there was a trend of the DD genotype to be an independent risk factor (OR 1.4; p = 0.08). No differences in DD genotype prevalence according to exogenous risk factors were found. Coinheritance of FV G1691A, PT G20210A mutation, and PS deficiency with the DD genotype increased the relative risk of VTE. Thus, the ACE DD genotype is a moderate risk factor of hereditary thrombophilia. Exogenous risk factors did not alter the manifestation of VTE among carriers of the DD genotype, whereas coinheritance of the DD genotype with the aforementioned defects increased the risk for VTE considerably.

 
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