血管紧张素转化酶 I/D 多态性与慢性阻塞性肺疾病。
Angiotensin-converting enzyme I/D polymorphism in chronic obstructive pulmonary disease.
机构信息
Medizinische Klinik und Poliklinik II, Pulmonary Division, Department of Medicine, Universitätsklinikum Bonn, Bonn, Germany.
出版信息
Eur J Med Res. 2009 Dec 7;14 Suppl 4(Suppl 4):177-81. doi: 10.1186/2047-783x-14-s4-177.
STUDY OBJECTIVE
The etiology of chronic obstructive lung disease (COPD) is unclear. It is supposed to be the product of an exogenous antigenic stimulus, such as tobacco smoke, and an endogenous genetic susceptibility. The angiotensin-converting enzyme (ACE) gene contains a polymorphism based on the presence (insertion [I]) or absence (deletion [D]) of a 287-bp nonsense domain, resulting in three different genotypes (II, ID and DD). The aim of the study was to find out whether the ACE gene polymorphism can determine the course of COPD.
PATIENTS AND DESIGN
We genotyped 152 Caucasian patients with COPD and 158 healthy controls for the ACE (I/D) polymorphism. We divided the COPD group into one group of 64 patients with a stable course of disease, defined as less than three hospitalizations over the last three years due to COPD, and another group of 88 patients with an instable course with more than three hospitalizations.
RESULTS
The I-allele was significantly associated with an increased risk for COPD in a dominant model (OR 1.67 (95% CI 1.00 to 2.78), p=0.048), but not in a recessive or co-dominant model. Moreover, the I-allele of ACE (I/D) was significantly increased in patients with a stable course of COPD (p=0.012) compared with controls. In a dominant model (II/ID v DD) we found an even stronger association between the I-allele and a stable course of COPD (OR 3.24 (95% CI 1.44 to 7.31), p=0.003).
CONCLUSION
These data suggest that the presence of an ACE I-allele determines a stable course of COPD.
研究目的
慢性阻塞性肺病（COPD）的病因尚不清楚。它被认为是外源性抗原刺激的产物，如烟草烟雾，以及内源性遗传易感性。血管紧张素转换酶（ACE）基因含有基于存在（插入[I]）或不存在（缺失[D]）287bp 无意义结构域的多态性，导致三种不同的基因型（II、ID 和 DD）。本研究旨在探讨 ACE 基因多态性是否能确定 COPD 的病程。
患者和设计
我们对 152 例 COPD 患者和 158 例健康对照者进行 ACE（I/D）多态性基因分型。我们将 COPD 组分为一组 64 例疾病稳定的患者，定义为过去三年因 COPD 住院少于三次，另一组 88 例疾病不稳定的患者，住院超过三次。
结果
在显性模型中，I 等位基因与 COPD 风险增加显著相关（OR 1.67（95%CI 1.00 至 2.78），p=0.048），但在隐性或共显性模型中则不相关。此外，在稳定型 COPD 患者中，ACE（I/D）的 I 等位基因显著增加（p=0.012）与对照组相比。在显性模型（II/ID v DD）中，我们发现 I 等位基因与稳定型 COPD 之间的相关性更强（OR 3.24（95%CI 1.44 至 7.31），p=0.003）。
结论
这些数据表明 ACE I 等位基因的存在决定了 COPD 的稳定病程。
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