J Korean Med Assoc.  2006 Apr;49(4):297-304. 10.5124/jkma.2006.49.4.297.

Definition, Epidemiology and Pathogenesis of Chronic Obstructive Pulmonary Disease

• Kim HJ

• KMID: 1958283
• DOI: http://doi.org/10.5124/jkma.2006.49.4.297

Abstract

Aworking definition of chronic obstructive pulmonary disease (COPD) is given within the GOLD Global strategy as a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. There is consensus that there has been a world-wide increase in COPD, reflecting increases in cigarette smoking, especially in developing countries. According to the Global Burden of Disease Study, in terms of lost disability-adjusted life years, COPD was ranked the 12th in 1990 and predicted to rise to the 5th ranking by 2020 and COPD was the sixth most common cause of death in the world in 1990 and will rise to the third most common by 2020. COPD is characterized by exaggeration of the normal inflammation response to irritant such as cigarette smoke. The mechanisms for this amplification of inflammation in COPD are not yet certain, but may be determined by genetic factors, latent viruses and impaired histone deacetylase activity. In addition to inflammation, extracellular matrix proteolysis. Cell death and ineffective repair are thought to be important in the pathogenesis of COPD.

Keyword

Chronic obstructive pulmonary disease; Definition; Epidemiolgy; Pathogenesis; Chronic inflammation

MeSH Terms

Cause of Death
Cell Death
Consensus
Developing Countries
Epidemiology*
Extracellular Matrix
Gases
Histone Deacetylases
Inflammation
Lung
Proteolysis
Pulmonary Disease, Chronic Obstructive*
Smoke
Smoking
Tobacco Products
Gases
Histone Deacetylases
Smoke

Figure

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  Figure 1 Definition of COPD

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  Figure 2 Diseases included with COPD

Reference

1. Global Initiative for Chronic Obstructive Lung Disease (GOLD): Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease NHLBI/WHO Workshop Report. National Institutes of Health (NIH), National Heart Lung and Blood Institute (NHLBI), World Health Organiztion (WHO). 2001, 2003, 2004 and update in 2005. www.goldcopd.com/workshop/index.html.

2. National Institute for Clinical Excellence (NICE). Chronic Obstructive Pulmonary Disease: national clinical guideline for management of chronic obstructive pulmonary disease in adults in primary and secondary care. Thorax. 2004. 59:Suppl 1. 1–232.

3. Gross NJ. Extrapulmonary effects of chronic obstructive pulmonary disease. Curr Opin Pulm Med. 2001. 7:84–92.

4. Hansel TT, Barnes PJ. An Atlas of Chronic Obstructive Pulmonary Disease COPD. 2004. 1st ed. New York: Parthenon Publishing;3–4.

5. Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000. 343:269–280.

6. Halbert RJ, Isonaka S, George D, Iqbal A. Interpreting COPD prevalence estimates: what is the true burden of disease? Chest. 2003. 123:1684–1692.

7. Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J. 1977. 1:1645–1648.

8. National Center for Health Statistics. Current estimates from the National Health Interview Survey, United States, 1995 Department of Health and Human Sevices, Public Health Service. Vital Health Stat. 1995. 96:1527.

9. Murray CJ, Lopez AD. Evidence-based health policy-lessons from the Global Burden Study. Science. 1996. 274:740–743.

10. Gulsvik A. Mortality in and prevalence of chronic obstructive pulmonary disease. Monaldi Arch Chest Dis. 1999. 54:160–162.

11. Regional COPD Working Group. COPD prevalence in 12 Asia-Pacific countries and regions: projections based on the COPD prevalence estimation model. Respirology. 2003. 8:192–198.

12. de Marco R, Accordini S, Cerveri I, Corsico A, Sunyer J, Burney P, et al. An international survey of chronic obstructive pulmonary disease in young adults according to GOLD stages. Thorax. 2004. 59:120–125.

13. Kim DS, Kim YS, Jung K-S, Chang JH, Lim C-M, Lew WJ, et al. Prevalence of Chronic Obstructive Pulmonary Disease in Korea: A Population-based Spirometry Survey. Am J Respir Crit Care Med. 2005. 172:842–847.

14. Slusarcick A, McCaig L. National Hospital Ambulatory Medical Care Survey: 1988 outpatient department summary. Adv Data. 2000. 317:1–23.

15. Mannino DM. COPD: epidemiology, prevalence, morbidity and mortality, and disease heterogeneity. Chest. 2002. 121:121S–126S.

16. Popovic JR, Kozak LJ. National hospital discharge survey: annnual summary, 1998. Vital Health Stat 13. 2000. 148:1–194.

17. Mannino DM, Homa DM, Akinbami LJ, Ford ES, Redd SC. Chronic obstructive pulmonary disease surveillance-United States, 1971~2000. Respir Care. 2002. 47:1184–1199.

18. Hurd S. The Impact of COPD on Lung Health Worldwide: Epidemiology and Incidence. Chest. 2000. 117:1S–4S.

20. Murray CJ, Lopez AD. Mortality by cause for eight regions of the world : Global Burden of Disease Study. Lancet. 1997. 339:1269–1276.

21. Murray CJ, Lopez AD. Alternative projections of mortality and disability by cause 1990~2020: Global Burden of Disease Study. Lancet. 1997. 349:1498–1504.

22. Barnes PJ. Molecular genetics of chronic obstructive pulmonary disease. Thorax. 1999. 54:245–252.

23. Meshi B, Vitalis TZ, Ionescu D, Elliott WM, Liu C, Wang XD, et al. Emphysematous lung destruction by cigarette smoke. The effects of latent adenoviral infection on the lung inflammatory response. Am J Respir Cell Mol Biol. 2002. 26:52–57.

24. Ito K, Lim S, Caramori G, Chung KF, Barnes PJ, Adock IM. Cigarette smoking reduces histone deacetylase 2 expression, enhances cytokine expression and inhibits glucocorticoid actions in alveolar macrophages. FASEB J. 2001. 15:1110–1112.

25. Laurell CB, Eriksson S. The electrophoretic alpha-globulin pattern of serum in alpha-antitrypsin deficiency. Scand J Clin Invest. 1963. 15:132–140.

26. Stockley RA. The role of proteinases in the pathogenesis of chronic bronchitis. Am J Respir Crit Care Med. 1994. 150:S109–S113.

27. Shapiro SD. Elastolytic metalloproteinases produced by human mononuclear phagocytes. Potential roles in destructive lung disease. Am J Respir Crit Care Med. 1994. 150:S160–S164.

28. MacNee W, Rahman I. Is oxidative stress central to the pathogenesis of chronic obstructive pulmonary disease? Trends Mol Med. 2001. 7:55–62.

29. Aoshiba K, Yokohori N, Nagai A. Alveolar wall apoptosis causes lung destruction and emphysematous changes. Am J Respir Cell Mol Biol. 2003. 28:555–562.

30. Kasahari Y, Tuder RM, Cool CD, Lynch DA, Flores SC, Voelkel NF. Inhibition of VEGF receptors causes lung cell apoptosis and emphysema. J Clin Invest. 2000. 106:1311–1319.

31. Massaro GD, Massaro D. Retinoic acid treatment abrogates elastase elastase-induced pulmonary emphysema in rats. Nat Med. 1997. 6:675–677.