title: The role of ace gene polymorphism in the development of angioedema secondary to angiotensin converting enzyme inhibitors and angiotensin II receptor blockers.
abstract: 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.
  
  
  CONCLUSIONS
  Our results showed that ACE gene polymorphism has no effect on ACEi or ATRB induced angioedema.
authors.affiliation: Department Internal Medicine and Division of Allergy. Gülhane Military Medical Academy and Medical School, Ankara, Turkey. gulec_mustafa@yahoo.com
authors.forename: M
authors.initials: M
authors.lastname: Gulec
authors.forename: Z
authors.initials: Z
authors.lastname: Caliskaner
authors.forename: Y
authors.initials: Y
authors.lastname: Tunca
authors.forename: S
authors.initials: S
authors.lastname: Ozturk
authors.forename: E
authors.initials: E
authors.lastname: Bozoglu
authors.forename: D
authors.initials: D
authors.lastname: Gul
authors.forename: F
authors.initials: F
authors.lastname: Erel
authors.forename: O
authors.initials: O
authors.lastname: Kartal
authors.forename: M
authors.initials: M
authors.lastname: Karaayvaz
mesh_terms: D000328:Adult; D000368:Aged; D000799:Angioedema / Q000139:chemically induced / Q000235:genetics*; D000804:Angiotensin II / Q000378:metabolism; D047228:Angiotensin II Type 1 Receptor Blockers / Q000008:administration & dosage / Q000009:adverse effects*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A