• M Gulec, Z Caliskaner, Y Tunca, S Ozturk, E Bozoglu, D Gul, F Erel, O Kartal, and M Karaayvaz.
• Department Internal Medicine and Division of Allergy. Gülhane Military Medical Academy and Medical School, Ankara, Turkey. gulec_mustafa@yahoo.com
• Allergol Immunopathol (Madr). 2008 May 1;36(3):134-40.

BackgroundAngiotensin 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.ObjectiveThe aim of this study was to investigate whether the relationship between ACE gene polymorphism and ACEi induced angioedema is present or not.MethodsACE 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).ResultsID 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.ConclusionOur results showed that ACE gene polymorphism has no effect on ACEi or ATRB induced angioedema.

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