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.
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-oedemapatients 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.
Authors: F Soubrier; F Alhenc-Gelas; C Hubert; J Allegrini; M John; G Tregear; P Corvol Journal: Proc Natl Acad Sci U S A Date: 1988-12 Impact factor: 11.205
Authors: Itahisa Marcelino-Rodriguez; Ariel Callero; Alejandro Mendoza-Alvarez; Eva Perez-Rodriguez; Javier Barrios-Recio; Jose C Garcia-Robaina; Carlos Flores Journal: Front Genet Date: 2019-09-27 Impact factor: 4.599
Authors: Retsilisitsoe R Moholisa; Brian R Rayner; E Patricia Owen; Sylva L U Schwager; Joalice S Stark; Motassim Badri; Clint L Cupido; Edward D Sturrock Journal: J Clin Hypertens (Greenwich) Date: 2013-04-11 Impact factor: 3.738
Authors: Haivin Aziz Ali; Anne Fog Lomholt; Seyed Hamidreza Mahmoudpour; Thorbjørn Hermanrud; Anette Bygum; Christian von Buchwald; Marianne Antonius Jakobsen; Eva Rye Rasmussen Journal: PLoS One Date: 2019-11-11 Impact factor: 3.240