|
 |
|
|||||||
|
|||||||||
Copyright ©ERS Journals Ltd 2007
Definition, epidemiology and natural history of COPD
1 Pulmonary Environmental Epidemiology Unit, CNR Institute of Clinical Physiology, and 2 Cardiothoracic Dept, University of Pisa, Pisa, Italy, 3 Arizona Clinical Research Training Program, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ, USA.
CORRESPONDENCE: G. Viegi, CNR Institute of Clinical Physiology, Via Trieste 41, 56126 Pisa, Italy. Fax: 39 050502031. E-mail: viegig{at}ifc.cnr.it
Keywords: Air pollution, chronic obstructive pulmonary disease clinical/basic investigations, cor pulmonale, epidemiology of asthma/chronic obstructive pulmonary disease, smoking, spirometry
Received: July 4, 2007
Accepted August 13, 2007
Chronic obstructive pulmonary disease (COPD) is the fifth cause of morbidity and mortality in the developed world and represents a substantial economic and social burden. Patients experience a progressive deterioration up to end-stage COPD, characterised by very severe airflow limitation, severely limited and declining performance status with chronic respiratory failure, advanced age, multiple comorbidities and severe systemic manifestations/complications.
COPD is frequently underdiagnosed and under-treated. Today, COPD develops earlier in life and is less gender specific. Tobacco smoking is the major risk factor for COPD, followed by occupation and air pollution. Severe deficiency for
Without major efforts in prevention, there will be an increasing proportion of end-stage patients who can live longer through long-term oxygen therapy and assisted ventilation, but with elevated suffering and huge costs. Smoking prevention and smoking cessation are the most important epidemiological measurements to counteract chronic obstructive pulmonary disease epidemics.
1-antitrypsin is rare; several phenotypes are being associated with elevated risk for COPD in the presence of risk factor exposure. Any patient presenting with cough, sputum production or dyspnoea should be assessed by standardised spirometry. Continued exposure to noxious agents promotes a more rapid decline in lung function and increases the risk for repeated exacerbations, eventually leading to end-stage disease.
This article has been cited by other articles:
|
|
 |
|
  O. Laurent, G. Pedrono, L. Filleul, C. Segala, A. Lefranc, C. Schillinger, E. Riviere, and D. Bard Influence of Socioeconomic Deprivation on the Relation Between Air Pollution and {beta}-Agonist Sales for Asthma Chest, March 1, 2009; 135(3): 717 - 723. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Michelozzi, G. Accetta, M. De Sario, D. D'Ippoliti, C. Marino, M. Baccini, A. Biggeri, H. R. Anderson, K. Katsouyanni, F. Ballester, et al. High Temperature and Hospitalizations for Cardiovascular and Respiratory Causes in 12 European Cities Am. J. Respir. Crit. Care Med., March 1, 2009; 179(5): 383 - 389. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Chaouat, R. Naeije, and E. Weitzenblum Pulmonary hypertension in COPD Eur. Respir. J., November 1, 2008; 32(5): 1371 - 1385. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Vestbo, W. Anderson, H. O. Coxson, C. Crim, F. Dawber, L. Edwards, G. Hagan, K. Knobil, D. A. Lomas, W. MacNee, et al. Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE) Eur. Respir. J., April 1, 2008; 31(4): 869 - 873. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |