Potential genetic risk factors in angiotensin-converting enzyme-inhibitor-induced angio-oedema

Abstract

Aims The pathophysiology of angiotensin-converting enzyme inhibitor (ACEi)-induced angio-oedema remains unclear. We have investigated the impact of ACE insertion/deletion (I/D) polymorphism in combination with serum ACE activity as well as the bradykinin B2 receptor 2/3 and c.C181T polymorphisms. Methods We analysed the ACE I/D as well as bradykinin B2 (2/3 and C181T) receptor polymorphisms in 65 patients with documented episodes of ACEi-induced angio-oedema and 65 patients matched for age and sex being under ACEi treatment without history of angio-oedema. Furthermore, we determined serum ACE activity in 47 of the 65 angio-oedema patients 3 months after the angio-oedema attack and compared these values with 51 healthy individuals (control II). Results No risk association was identified between ACE I/D (I-allele: 0.42 vs. 0.41, D-allele: 0.58 vs. 0.59; P = 0.095) or bradykinin B2 receptor polymorphisms and the development of angio-oedema during ACEi treatment. We found a trend of lower serum ACE activity in ACE I/I genotypes in comparison with control II (I/I: 28 ± 4.5 vs. 33 ± 1.8 U l-1; ID: 39 ± 3.3 vs. 41 ± 1 U l-1; DD: 56 ± 6.7 vs. 52 ± 1.8 U l-1; P = 0.9). Conclusions Our data suggest that polymorphism of ACE I/D and the bradykinin B2 receptor polymorphisms are not involved in the development of ACEi-induced angio-oedema when considered individually. Further studies should be carried out to clarify whether a combination of these polymorphisms might be a risk factor for ACEi-induced angio-oedema. © 2010 The British Pharmacological Society.