Article date: February 2010
By: Murat Bas, Thomas K. Hoffmann, Bernd Tiemann, Vu Thao‐Vi Dao, Christos Bantis, Vera Balz, Hans‐Jürgen Schultz‐Coulon, Thomas Stark, Patrick Schuler, Jens Greve, Katrin Ivens, Henning Bier, Georg Kojda, in Volume 69, Issue 2, pages 179-186
WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT
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.
DOI: 10.1111/j.1365-2125.2009.03567.x
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