Risk factors for the development of chronic obstructive pulmonary disease

Channing Laboratory, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Medical Clinics of North America (Impact Factor: 2.61). 06/1996; 80(3):501-22. DOI: 10.1016/S0025-7125(05)70451-X
Source: PubMed


Cigarette smoking clearly has been shown to be the major environmental risk factor predisposing to the development of COPD. Occupational exposures to dust and fumes, air pollution, passive smoke exposure, childhood respiratory infections, and diet may also contribute. Airway hyperresponsiveness is a risk factor for the development of decline in FEV1, but its role in the development of COPD remains uncertain. Alpha1-antitrypsin deficiency is an important genetic risk factor for COPD in the small minority of COPD patients who inherit this deficiency. Other genetic factors are likely involved but have not yet been identified. Elucidation of additional genetic risk factors may provide useful insights into the pathogenesis of COPD. Potential interactions between the various environmental and genetic risk factors may be extremely important in determining the variable development of COPD.

1 Follower
5 Reads
  • Source
    • "Chronic obstructive pulmonary disease (COPD) is a condition characterised by impaired airflow to the lungs that worsens over time [1]. The primary risk factor for COPD is long-term exposure to noxious particles and gases, in particular from cigarette smoking, which has been shown to trigger inflammation and abnormal immune responses in the small airways [2]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) independently associates with an increased risk of coronary artery disease (CAD), but it has not been fully investigated whether this co-morbidity involves shared pathophysiological mechanisms. To identify potential common pathways across the two diseases, we tested all recently published single nucleotide polymorphisms (SNPs) associated with human lung function (spirometry) for association with carotid intima-media thickness (cIMT) in 3,378 subjects with multiple CAD risk factors, and for association with CAD in a case-control study of 5,775 CAD cases and 7,265 controls. SNPs rs2865531, located in the CFDP1 gene, and rs9978142, located in the KCNE2 gene, were significantly associated with CAD. In addition, SNP rs9978142 and SNP rs3995090 located in the HTR4 gene, were associated with average and maximal cIMT measures. Genetic risk scores combining the most robustly spirometry-associated SNPs from the literature were modestly associated with CAD, (odds ratio (OR) (95% confidence interval (CI95) = 1.06 (1.03, 1.09); P-value = 1.5×10-4, per allele). In conclusion, our study suggests that some genetic loci implicated in determining human lung function also influence cIMT and susceptibility to CAD. The present results should help elucidate the molecular underpinnings of the co-morbidity observed across COPD and CAD.
    PLoS ONE 08/2014; 9(8):e104082. DOI:10.1371/journal.pone.0104082 · 3.23 Impact Factor
  • Source
    • "Also, other extrapulmonary effects, such as weight loss, nutritional abnormalities, skeletal muscle dysfunction influence the severity of the disease. Apart from the genetic background (hereditary alpha-1 antitrypsin deficiency) [7] cigarette smoke is a crucial environmental factor in COPD development [8]; it is responsible for airway inflammation and further oxidant/antioxidant imbalance (oxidative stress) causing amplification of lung inflammation. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The increased morbidity, mortality, and ineffective treatment associated with the pathogenesis of chronic inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD) have generated much research interest. The key role is played by phospholipases from the A2 superfamily: enzymes which are involved in inflammation through participation in pro- and anti-inflammatory mediators production and have an impact on many immunocompetent cells. The 30 members of the A2 superfamily are divided into 7 groups. Their role in asthma and COPD has been studied in vitro and in vivo (animal models, cell cultures, and patients). This paper contains complete and updated information about the involvement of particular enzymes in the etiology and course of asthma and COPD.
    Mediators of Inflammation 05/2013; 2013(3):793505. DOI:10.1155/2013/793505 · 3.24 Impact Factor
  • Source
    • "The relationship between smoking and COPD is not absolute. COPD can occur in lifelong non-smokers;2 indeed more than 15% of subjects worldwide who die from COPD are non-smokers. Moreover, only approximately 30% of subjects who have a significant smoking history go on to develop clinically significant COPD.3 "
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease is a varied condition when examined from a number of different perspectives including factors which influence disease development, pathological process and clinical features. There may be a complex interaction between the degree by which each of these processes influences the development of COPD and the subsequent clinical phenotype with which the patient presents. The varied host response and subsequent clinical phenotype has generated much interest in recent years. It is possible that failure of treatment to impact on mortality and reverse the disease process is because of the heterogeneous nature of the condition. Identification and targeted treatment of clinical and pathological phenotypes within the broad spectrum of COPD may therefore improve outcome. This article will review previous work which has attempted to phenotype COPD and identify if specific treatment for these phenotypes has been shown to be of benefit. It will examine the work on pathological processes and clinical manifestations, both pulmonary and systemic, and will focus on pharmacological therapies.
    International Journal of COPD 09/2009; 4:321-35. · 3.14 Impact Factor
Show more

Similar Publications