The role of ace gene polymorphism in the development of angioedema secondary to angiotensin converting enzyme inhibitors and angiotensin II receptor blockers

التفاصيل البيبلوغرافية
العنوان: The role of ace gene polymorphism in the development of angioedema secondary to angiotensin converting enzyme inhibitors and angiotensin II receptor blockers
المؤلفون: Zafer Çalişkaner, Mustafa Gulec, Fuat Erel, Sami Öztürk, Y. Tunca, E. Bozoglu, Mehmet Karaayvaz, Özgür Kartal, D. Gul
المصدر: Allergologia et Immunopathologia. 36:134-140
بيانات النشر: Codon Publications, 2008.
سنة النشر: 2008
مصطلحات موضوعية: Adult, Male, Pulmonary and Respiratory Medicine, Ace gene polymorphism, medicine.medical_specialty, Genotype, Immunology, Bradykinin, Angiotensin-Converting Enzyme Inhibitors, Angiotensin II Receptor Blockers, Peptidyl-Dipeptidase A, chemistry.chemical_compound, Internal medicine, medicine, Humans, Immunology and Allergy, Genetic Predisposition to Disease, cardiovascular diseases, Angioedema, Aged, Polymorphism, Genetic, biology, business.industry, Angiotensin II, Angiotensin-converting enzyme, General Medicine, Middle Aged, Chromosome 17 (human), Endocrinology, chemistry, biology.protein, Female, Gene polymorphism, medicine.symptom, business, Angiotensin II Type 1 Receptor Blockers
الوصف: 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.
تدمد: 0301-0546
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9966bab7f60644fd5cb50e5efafa9515Test
https://doi.org/10.1016/s0301-0546Test(08)72537-0
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....9966bab7f60644fd5cb50e5efafa9515
قاعدة البيانات: OpenAIRE