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首页> 外文期刊>The journal of clinical hypertension. >Association of B2 Receptor Polymorphisms and ACE Activity With ACE Inhibitor-Induced Angioedema in Black and Mixed-Race South Africans
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Association of B2 Receptor Polymorphisms and ACE Activity With ACE Inhibitor-Induced Angioedema in Black and Mixed-Race South Africans

机译：黑人和混合种族南非人中B2受体多态性和ACE活性与ACE抑制剂引起的血管性水肿的关联

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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, B2 receptor -9/+9 polymorphism, and B2 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 B2 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 B2 -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 B2 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 B2 -9 allele and reduced ACE activity are associated with both ACE-AE and ACE-cough.
机译：血管紧张素转换酶（ACE）抑制剂是用于治疗高血压，充血性心力衰竭和糖尿病性肾病的一线疗法。 ACE抑制剂与不良副作用有关，例如持续性干咳（ACE-咳嗽），以及极少数危及生命的血管性水肿（ACE-AE）。作者研究了ACE I / D多态性与血清ACE活性，B2受体-9 / + 9多态性和B2受体C-58T单核苷酸多态性（SNP）结合对ACE-AE和ACE-咳嗽发生的影响。比较了ACE-AE，ACE-咳嗽和ACE抑制剂暴露对照组的ACE I / D频率以及B2受体+ 9 / -9和C-58T多态性，并测量了血清ACE活性。有52例ACE-AE，36例ACE-咳嗽和77例对照。基因分型显示当B2 -9等位基因与ACE抑制剂诱导的AE（62％vs 38％，P = .008）和ACE抑制剂诱导的咳嗽（61％vs 38％，P = .02）之间存在显着关联与控件相比。 ACE I / D多态性以及B2 C-58T SNP与ACE诱发的AE和咳嗽之间无显着关联。与ACE-AE（34.5±1.14 mU / mL vs 17.8±0.86 mU / mL，P = .0001）和ACE咳嗽（34.5±1.14 mU / mL vs 23.3±1.88 mU）的患者相比，对照组的ACE活性明显更高/mL，P=.0001）。因此，我们的数据表明，B2 -9等位基因和降低的ACE活性与ACE-AE和ACE-咳嗽有关。

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