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Gene Review

COPD1  -  Chronic obstructive pulmonary disease QTL 1

Homo sapiens

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Disease relevance of COPD1

  • Inflammatory/immune response mediators and the overproduction of mucus characterize chronic airway diseases: asthma, chronic obstructive pulmonary diseases (COPD), or cystic fibrosis (CF) [1].
  • Mucin overproduction in chronic airway diseases and secretory cell metaplasia in animal model systems are reviewed in section ii and addressed in disease-specific subsections on asthma, COPD, and CF [1].
  • Three case definitions of COPD were used: symptoms of chronic bronchitis (667 subjects), physician-diagnosed emphysema reported by the subject (185 subjects), and spirometrically detected COPD (197 subjects) [2].
  • The rate of excretion of all metabolites in the patients with COPD but no clinical evidence of pulmonary hypertension was similar to that in the normal controls [3].
  • CONCLUSIONS: Independently of other risk factors, regular cigar smoking can increase the risk of coronary heart disease, COPD, and cancers of the upper aerodigestive tract and lung [4].

Psychiatry related information on COPD1


High impact information on COPD1


Chemical compound and disease context of COPD1


Biological context of COPD1

  • These results indicate that the tidal volume and respiratory timing responses to flow loads are impaired in some patients with COPD [18].
  • The hypothesis that patients with chronic obstructive pulmonary disease (COPD) have chronic inspiratory muscle fatigue was tested in an effectiveness trial in which negative pressure ventilation (NPV) was used to produce inspiratory muscle rest [19].
  • To identify genetic determinants of quantitative spirometric phenotypes, an autosomal 10-cM genomewide scan of short tandem repeat (STR) polymorphic markers was performed in 72 pedigrees (585 individuals) ascertained through probands with severe early-onset COPD [20].
  • COPD is defined by irreversible airflow obstruction; airflow obstruction is typically determined by reductions in quantitative spirometric indices, including forced expiratory volume at 1 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC) [20].
  • Association of five of these SNPs with COPD was replicated in a case-control analysis, with cases from the National Emphysema Treatment Trial and controls from the Normative Aging Study. Family-based and case-control haplotype analyses supported similar regions of association within the SERPINE2 gene [21].

Anatomical context of COPD1

  • We conclude that NPV as used in this study is difficult to apply and ineffective when used with the aim of resting the respiratory muscles in patients with stable COPD [19].
  • The main characteristic of COPD is the continued inflammation caused by the sustained influx of macrophages and neutrophils into the lung [22].
  • Such a pharmacological strategy would provide a mechanism with which to inhibit leukocyte recruitment and, hence, reduce the inflammatory profile in COPD, which is currently unaffected by pharmacotherapy [23].
  • Inspiratory filling of the right ventricle is not hampered, but rather is exaggerated in patients with COPD and pulsus paradoxus, and left ventricular stroke volume is reduced during inspiration [24].
  • CCR3 antagonists (which block eosinophil chemotaxis) and CXCR2 antagonists (which block neutrophil and monocyte chemotaxis) are in clinical development for asthma and COPD, respectively [25].

Associations of COPD1 with chemical compounds

  • The basal level of cortisol exceeded the normal one in all patients' groups, particularly in COPD1 (by 1.6 times; p < 0.05) [26].
  • We administered theophylline and placebo orally to 40 ambulatory COPD patients in a double-blind, crossover manner [13].
  • PATIENTS--Forty-eight patients with steroid-dependent asthma or COPD who had shown a decline in forced expiratory volume in 1 second (FEV1) of at least 80 mL per year and at least one exacerbation per year during the first 2 years of bronchodilator treatment [27].
  • On a resistance of 10 cm H2O/liter per s, the highest load that could be tolerated by all COPD patients, the increase in PCO2 ranged from 1 to 11 mm Hg, while none of the normal subjects retained CO2 [18].
  • Combined salmeterol and fluticasone for COPD [28].

Analytical, diagnostic and therapeutic context of COPD1

  • Those who smoked cigars (1546 men) and those who did not (16,228) were followed from 1971 through the end of 1995 for a first hospitalization for or death from a major cardiovascular disease or COPD, and through the end of 1996 for a diagnosis of cancer [4].
  • The presence of COPD was assessed by a questionnaire on respiratory symptoms and by spirometry [2].
  • The primary end point was treatment failure, defined as death from any cause or the need for intubation and mechanical ventilation, readmission to the hospital for COPD, or intensification of drug therapy [29].
  • PATIENTS: Fifty patients with acute exacerbation of COPD or severe CPE who were treated with NIV for at least 2 hours and 50 patients treated with mechanical ventilation between 1993 and 1998 (controls), matched on diagnosis, Simplified Acute Physiology Score II, Logistic Organ Dysfunction score, age, and no contraindication to NIV [30].
  • OBJECTIVE--A meta-analysis of randomized trials was performed to estimate the effectiveness of antibiotics in treating exacerbations of chronic obstructive pulmonary disease (COPD) [10].


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  2. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. Atherosclerosis Risk in Communities Study Investigators. Shahar, E., Folsom, A.R., Melnick, S.L., Tockman, M.S., Comstock, G.W., Gennaro, V., Higgins, M.W., Sorlie, P.D., Ko, W.J., Szklo, M. N. Engl. J. Med. (1994) [Pubmed]
  3. An imbalance between the excretion of thromboxane and prostacyclin metabolites in pulmonary hypertension. Christman, B.W., McPherson, C.D., Newman, J.H., King, G.A., Bernard, G.R., Groves, B.M., Loyd, J.E. N. Engl. J. Med. (1992) [Pubmed]
  4. Effect of cigar smoking on the risk of cardiovascular disease, chronic obstructive pulmonary disease, and cancer in men. Iribarren, C., Tekawa, I.S., Sidney, S., Friedman, G.D. N. Engl. J. Med. (1999) [Pubmed]
  5. Smoking cessation in patients with chronic obstructive pulmonary disease: a double-blind, placebo-controlled, randomised trial. Tashkin, D., Kanner, R., Bailey, W., Buist, S., Anderson, P., Nides, M., Gonzales, D., Dozier, G., Patel, M.K., Jamerson, B. Lancet (2001) [Pubmed]
  6. Depressive symptoms and chronic obstructive pulmonary disease: effect on mortality, hospital readmission, symptom burden, functional status, and quality of life. Ng, T.P., Niti, M., Tan, W.C., Cao, Z., Ong, K.C., Eng, P. Arch. Intern. Med. (2007) [Pubmed]
  7. Long-term effects of almitrine bismesylate on oxygenation during wakefulness and sleep in chronic obstructive pulmonary disease. Gothe, B., Cherniack, N.S., Bachand, R.T., Szalkowski, M.B., Bianco, K.A. Am. J. Med. (1988) [Pubmed]
  8. Alcohol abuse: comparison of two methods for assessing its prevalence and associated morbidity in hospitalized patients. Umbricht-Schneiter, A., Santora, P., Moore, R.D. Am. J. Med. (1991) [Pubmed]
  9. The daily energy expenditure in stable chronic obstructive pulmonary disease. Hugli, O., Schutz, Y., Fitting, J.W. Am. J. Respir. Crit. Care Med. (1996) [Pubmed]
  10. Antibiotics in chronic obstructive pulmonary disease exacerbations. A meta-analysis. Saint, S., Bent, S., Vittinghoff, E., Grady, D. JAMA (1995) [Pubmed]
  11. Acute or chronic respiratory failure. Assessment and management of patients with COPD in the emergency setting. Schmidt, G.A., Hall, J.B. JAMA (1989) [Pubmed]
  12. The effect of terbutaline on cardiac function in patients with stable chronic obstructive lung disease. Sunderrajan, E.V., Byron, W.A., McKenzie, W.N., Hurst, D.J., Allegro, M.M., Thakur, V.M., Holmes, R.A. JAMA (1983) [Pubmed]
  13. Treatment of chronic obstructive pulmonary disease with orally administered theophylline. A double-blind, controlled study. Alexander, M.R., Dull, W.L., Kasik, J.E. JAMA (1980) [Pubmed]
  14. Research applications and implications of adenosine in diseased airways. Spicuzza, L., Bonfiglio, C., Polosa, R. Trends Pharmacol. Sci. (2003) [Pubmed]
  15. PDE4 inhibition: a novel approach for the treatment of inflammatory bowel disease. Banner, K.H., Trevethick, M.A. Trends Pharmacol. Sci. (2004) [Pubmed]
  16. Ipratropium bromide in chronic bronchitis/emphysema. A review of the literature. Lakshminarayan, S. Am. J. Med. (1986) [Pubmed]
  17. Comparison of the anticholinergic bronchodilator ipratropium bromide with metaproterenol in chronic obstructive pulmonary disease. A 90-day multi-center study. Tashkin, D.P., Ashutosh, K., Bleecker, E.R., Britt, E.J., Cugell, D.W., Cummiskey, J.M., DeLorenzo, L., Gilman, M.J., Gross, G.N., Gross, N.J. Am. J. Med. (1986) [Pubmed]
  18. Mechanisms underlying CO2 retention during flow-resistive loading in patients with chronic obstructive pulmonary disease. Oliven, A., Kelsen, S.G., Deal, E.C., Cherniack, N.S. J. Clin. Invest. (1983) [Pubmed]
  19. Effect of negative pressure ventilation in severe chronic obstructive pulmonary disease. Shapiro, S.H., Ernst, P., Gray-Donald, K., Martin, J.G., Wood-Dauphinee, S., Beaupré, A., Spitzer, W.O., Macklem, P.T. Lancet (1992) [Pubmed]
  20. Genomewide linkage analysis of quantitative spirometric phenotypes in severe early-onset chronic obstructive pulmonary disease. Silverman, E.K., Palmer, L.J., Mosley, J.D., Barth, M., Senter, J.M., Brown, A., Drazen, J.M., Kwiatkowski, D.J., Chapman, H.A., Campbell, E.J., Province, M.A., Rao, D.C., Reilly, J.J., Ginns, L.C., Speizer, F.E., Weiss, S.T. Am. J. Hum. Genet. (2002) [Pubmed]
  21. The SERPINE2 Gene Is Associated with Chronic Obstructive Pulmonary Disease. Demeo, D.L., Mariani, T.J., Lange, C., Srisuma, S., Litonjua, A.A., Celedon, J.C., Lake, S.L., Reilly, J.J., Chapman, H.A., Mecham, B.H., Haley, K.J., Sylvia, J.S., Sparrow, D., Spira, A.E., Beane, J., Pinto-Plata, V., Speizer, F.E., Shapiro, S.D., Weiss, S.T., Silverman, E.K. Am. J. Hum. Genet. (2006) [Pubmed]
  22. The missing link: chemokine receptors and tissue matrix breakdown in COPD. Smit, J.J., Lukacs, N.W. Trends Pharmacol. Sci. (2006) [Pubmed]
  23. Chemokine receptors as therapeutic targets in chronic obstructive pulmonary disease. Donnelly, L.E., Barnes, P.J. Trends Pharmacol. Sci. (2006) [Pubmed]
  24. Echocardiographic study of the paradoxical arterial pulse in chronic obstructive lung disease. Settle, H.P., Engel, P.J., Fowler, N.O., Allen, J.M., Vassallo, C.L., Hackworth, J.N., Adolph, R.J., Eppert, D.C. Circulation (1980) [Pubmed]
  25. Cytokine-directed therapies for the treatment of chronic airway diseases. Barnes, P.J. Cytokine Growth Factor Rev. (2003) [Pubmed]
  26. Disorders of sex hormone status in patients with chronic obstructive pulmonary disease. Makarevich, A.E. Wiad. Lek. (2003) [Pubmed]
  27. Periodic treatment regimens with inhaled steroids in asthma or chronic obstructive pulmonary disease. Is it possible? van Schayck, C.P., van den Broek, P.J., den Otter, J.J., van Herwaarden, C.L., Molema, J., van Weel, C. JAMA (1995) [Pubmed]
  28. Combined salmeterol and fluticasone for COPD. Pakhale, S.S., Goldstein, R.S. Lancet (2003) [Pubmed]
  29. Effect of systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease. Department of Veterans Affairs Cooperative Study Group. Niewoehner, D.E., Erbland, M.L., Deupree, R.H., Collins, D., Gross, N.J., Light, R.W., Anderson, P., Morgan, N.A. N. Engl. J. Med. (1999) [Pubmed]
  30. Association of noninvasive ventilation with nosocomial infections and survival in critically ill patients. Girou, E., Schortgen, F., Delclaux, C., Brun-Buisson, C., Blot, F., Lefort, Y., Lemaire, F., Brochard, L. JAMA (2000) [Pubmed]
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