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      Impact of CYP1A1 Polymorphisms on Susceptibility to Chronic Obstructive Pulmonary Disease: A Meta-Analysis

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          Abstract

          Objective. Several studies have evaluated the association between CYP1A1 polymorphisms and the susceptibility of chronic obstructive pulmonary disease (COPD) with inconclusive results. We performed the first comprehensive meta-analysis to summarize the association between CYP1A1 polymorphisms and COPD risk. Method. A systematic literature search was conducted (up to April 2015) in five online databases: PubMed, EMBASE, China National Knowledge Infrastructure (CNKI), WeiPu, and WanFang databases. The strength of association was calculated by odds ratio (OR) and corresponding 95% confidence interval (CI). Results. Seven case-control studies with 1050 cases and 1202 controls were included. Our study suggested a significant association between the MspI polymorphism and COPD risk (CC versus TC + TT: OR = 1.57, CI: 1.09–2.26, P = 0.02; CC versus TT: OR = 1.73, CI: 1.18–2.55, P = 0.005). For the Ile/Val polymorphism, a significant association with COPD risk was observed (GG versus AG + AA: OR = 2.75, CI: 1.29–5.84, P = 0.009; GG versus AA: OR = 3.23, CI: 1.50–6.93, P = 0.003; AG versus AA: OR = 1.39, CI: 1.01–1.90, P = 0.04). Subgroup analysis indicated a significant association between the MspI variation and COPD risk among Asians (CC versus TC + TT: OR = 1.70, CI: 1.06–2.71, P = 0.03; CC versus TT: OR = 1.84, CI: 1.11–3.06, P = 0.02). Conclusion. The MspI and Ile/Val polymorphisms might alter the susceptibility of COPD, and MspI polymorphism might play a role in COPD risk among Asian population.

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          The natural history of chronic airflow obstruction.

          A prospective epidemiological study of the early stages of the development of chronic obstructive pulmonary disease was performed on London working men. The findings showed that forced expiratory volume in one second (FEV1) falls gradually over a lifetime, but in most non-smokers and many smokers clinically significant airflow obstruction never develops. In susceptible people, however, smoking causes irreversible obstructive changes. If a susceptible smoker stops smoking he will not recover his lung function, but the average further rates of loss of FEV1 will revert to normal. Therefore, severe or fatal obstructive lung disease could be prevented by screening smokers' lung function in early middle age if those with reduced function could be induced to stop smoking. Infective processes and chronic mucus hypersecretion do not cause chronic airflow obstruction to progress more rapidly. There are thus two largely unrelated disease processes, chronic airflow obstruction and the hypersecretory disorder (including infective processes).
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            Pulmonary and systemic oxidant/antioxidant imbalance in chronic obstructive pulmonary disease.

            An imbalance between oxidants and antioxidants is considered to play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). There is considerable evidence that an increased oxidative burden occurs in the lungs of patients with this disorder, and this may be involved in many of the pathogenic processes, such as direct injury to lung cells, mucus hypersecretion, inactivation of antiproteases, and enhancing lung inflammation through activation of redox-sensitive transcription factors. COPD is now recognized to have multiple systemic consequences, such as weight loss and skeletal muscle dysfunction. Moreover, it is appreciated that oxidative stress extends beyond the lung and may, through similar oxidative stress mechanisms as those in the lung, contribute to several of the systemic manifestations in COPD.
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              Risk factors for chronic obstructive pulmonary disease in a European cohort of young adults.

              Few studies have investigated the factors associated with the early inception of chronic obstructive pulmonary disease (COPD). We investigated COPD risk factors in an international cohort of young adults using different spirometric definitions of the disease. We studied 4,636 subjects without asthma who had prebronchodilator FEV(1)/FVC measured in the European Community Respiratory Health Survey both in 1991 to 1993 (when they were 20-44 yr old) and in 1999 to 2002. COPD was defined according to the Global Initiative for Chronic Obstructive Lung Disease fixed cut-off criterion (FEV(1)/FVC < 0.70), and two criteria based on the Quanjer and LuftiBus reference equations (FEV(1)/FVC less than lower limit of normal). COPD determinants were studied using two-level Poisson regression models. COPD incidence ranged from 1.85 (lower limit of normal [Quanjer]) to 2.88 (Global Initiative for Chronic Obstructive Lung Disease) cases/1,000/yr. Although about half of the cases had smoked less than 20 pack-years, smoking was the main risk factor for COPD, and it accounted for 29 to 39% of the new cases during the follow-up. Airway hyperresponsiveness was the second strongest risk factor (15-17% of new cases). Other determinants were respiratory infections in childhood and a family history of asthma, whereas the role of sex, age, and of being underweight largely depended on the definition of COPD used. COPD may start early in life. Smoking prevention should be given the highest priority to reduce COPD occurrence. Airway hyperresponsiveness, a family history of asthma, and respiratory infections in childhood are other important determinants of COPD. We suggest the need for a definition of COPD that is not exclusively based on spirometry.
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                Author and article information

                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi Publishing Corporation
                2314-6133
                2314-6141
                2015
                3 September 2015
                : 2015
                : 942958
                Affiliations
                1Department of Respiratory Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China
                2West China School of Medicine/West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China
                Author notes

                Academic Editor: Jill E. Larsen

                Article
                10.1155/2015/942958
                4573875
                b6d16c0a-6040-4df2-8cc0-62b6a1734602
                Copyright © 2015 Cheng-Di Wang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 May 2015
                : 31 July 2015
                : 18 August 2015
                Categories
                Review Article

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