Why the study?
Is ACE gene polymorphism associated with the development of angioedema secondary to ACE inhibitors or ARBs?
Is ACE gene polymorphism associated with the development of angioedema secondary to ACE inhibitors or ARBs?
ACE gene polymorphism (I/D) does not appear to be associated with the development of angioedema in patients treated with ACE inhibitors or ARBs.
No support for ACE I/D testing to stratify angioedema risk on ACEI/ARB; leaves open other genetic or mechanistic contributors.
BACKGROUND: Angiotensin Converting Enzyme inhibitors (ACEi) may cause angioedema, with an incidence of 0.1 % to 1 %, which may be life-threatening. ACEi induce angioedema by increasing the levels of bradykinin. Angiotensin II receptor blockers (ATRB), have a pharmacological profile similar to ACEi. The polymorphism of the ACE gene is based on the presence or absence of a 287-bp element on intron 16 on chromosome 17. The plasma level of ACE is related to gene polymorphism. ACE level in genotype DD is double that in genotype II. OBJECTIVE: The aim of this study was to investigate whether the relationship between ACE gene polymorphism and ACEi induced angioedema is present or not. METHODS: ACE gene polymorphism was investigated in patients with angioedema due to the use of ACEi or ATRB (n:32, group 1), in patients receiving ACEi or ATRB without angioedema (n:46, group 2), and healthy controls (n:96, group 3). RESULTS: ID polymorphism was the most frequent genotype in all groups, without any significant difference among the groups (p:0.868). ACE gene polymorphism was not related with the drugs used (ACEi or ATRB), localisation of angioedema, and female sex, in group 1. CONCLUSION: Our results showed that ACE gene polymorphism has no effect on ACEi or ATRB induced angioedema.
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Çalışkaner et al. (2008) studied this question.
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