Open AccessAssociation of B 2 Receptor Polymorphisms and ACE Activity With ACE Inhibitor–Induced Angioedema in Black and Mixed‐Race South Africans
Author(s) -
Moholisa Retsilisitsoe R.,
Rayner Brian R.,
Patricia Owen E.,
Schwager Sylva L. U.,
Stark Joalice S.,
Badri Motassim,
Cupido Clint L.,
Sturrock Edward D.
Publication year - 2013
Publication title -
the journal of clinical hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 67
eISSN - 1751-7176
pISSN - 1524-6175
DOI - 10.1111/jch.12104
Subject(s) - ace inhibitor , medicine , angiotensin converting enzyme , angioedema , endocrinology , blood pressure
Angiotensin‐converting enzyme ( ACE ) inhibitors are first‐line therapy for the treatment of hypertension, congestive heart failure, and diabetic nephropathy. ACE inhibitors are associated with adverse side effects such as persistent dry cough (ACE‐cough) and, rarely, life‐threatening angioedema (ACE‐ AE ). The authors investigated the influence of ACE I/D polymorphism in combination with serum ACE activity, B 2 receptor −9/+9 polymorphism, and B 2 receptor C‐58T single nucleotide polymorphism ( SNP) on the development of ACE ‐ AE and ACE ‐cough. The frequencies of ACE I/D as well as B 2 receptor +9/−9 and C‐58T polymorphisms were compared in patients with ACE ‐ AE , ACE ‐cough, and ACE inhibitor–exposed controls, and serum ACE activity was measured. There were 52 cases of ACE ‐ AE, 36 cases of ACE ‐cough, and 77 controls. The genotyping revealed a significant association between the B 2 −9 allele and ACE inhibitor–induced AE (62% vs 38%, P =.008), and ACE inhibitor –induced cough (61% vs 38%, P =.02) when compared with controls. There was no significant association between ACE I/D polymorphism as well as the B 2 C‐58T SNP with both ACE ‐induced AE and cough. ACE activity was significantly higher in controls compared with patients with ACE ‐AE (34.5±1.14 mU/mL vs 17.8±0.86 mU/mL, P =.0001) and ACE ‐cough (34.5±1.14 mU/mL vs 23.3±1.88 mU/mL, P =.0001). Thus, our data suggest that the B 2 −9 allele and reduced ACE activity are associated with both ACE ‐ AE and ACE ‐cough.