Potential genetic risk factors in angiotensin-converting enzyme-inhibitor-induced angio-oedema.
Br J Clin Pharmacol
; 69(2): 179-86, 2010 Feb.
Article
em En
| MEDLINE
| ID: mdl-20233181
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.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Polimorfismo Genético
/
Inibidores da Enzima Conversora de Angiotensina
/
Receptor B2 da Bradicinina
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Angioedema
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article