Gulec M, Caliskaner Z, Tunca Y, Ozturk S, Bozoglu E, Gul D, Erel F, Kartal O, Karaayvaz M
Department Internal Medicine and Division of Allergy. Gülhane Military Medical Academy and Medical School, Ankara, Turkey.
Allergol Immunopathol (Madr). 2008 May-Jun;36(3):134-40.
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.
The aim of this study was to investigate whether the relationship between ACE gene polymorphism and ACEi induced angioedema is present or not.
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).
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.
Our results showed that ACE gene polymorphism has no effect on ACEi or ATRB induced angioedema.
血管紧张素转换酶抑制剂（ACEi）可能会引起血管性水肿，发病率为0.1%至1%，这可能会危及生命。ACEi通过提高缓激肽水平来诱发血管性水肿。血管紧张素II受体阻滞剂（ATRB）具有与ACEi相似的药理学特征。ACE基因多态性基于17号染色体上16号内含子上287个碱基对元件的有无。ACE的血浆水平与基因多态性有关。DD基因型中的ACE水平是II基因型中的两倍。
本研究的目的是调查ACE基因多态性与ACEi诱发的血管性水肿之间是否存在关联。
对因使用ACEi或ATRB而发生血管性水肿的患者（n = 32，第1组）、接受ACEi或ATRB但未发生血管性水肿的患者（n = 46，第2组）以及健康对照者（n = 96，第3组）进行ACE基因多态性研究。
ID多态性是所有组中最常见的基因型，各组之间无显著差异（p = 0.868）。在第1组中，ACE基因多态性与所用药物（ACEi或ATRB）、血管性水肿的部位以及女性性别无关。
我们的结果表明，ACE基因多态性对ACEi或ATRB诱发的血管性水肿没有影响。
