The prevalence of COPD: using smoking rates to estimate disease frequency in the general population.

STUDY OBJECTIVES: To develop and validate a model based on smoking rates that will provide reliable estimates of the true prevalence of COPD that include both clinically detected and undetected patients. DESIGN: Model based on literature review. Age- and gender-specific rates of lung impairment by smoking status were applied to US smoking data. Resultant estimates were compared to the actual prevalence of obstructive airway disease as estimated by US national surveys. The model then was applied to estimate the prevalence of COPD in several European countries, where national data on undiagnosed lung disease do not exist. SETTING: The model was adapted from both a literature review and health-care data, and the analysis was applied to the United States and Europe. RESULTS: Using smoking rates, we estimate from our model that 15.3 million people who are > 40 years of age in the United States have COPD. The prevalence estimate, based on spirometric definitions for COPD in the same age group using the Third National Health and Nutrition Examination Survey (NHANES III), is 17.1 million people. NHANES III and other US national health-care surveys further suggest that only between 2.4 and 7 million people actually have COPD diagnosed; thus, the proportion of COPD that is currently being diagnosed in the United States is between 14% and 46% of all cases. Using smoking rates and our model, which was developed and validated for the United States, we calculated the prevalence of COPD for Germany (2.7 million people), the United Kingdom (3.0 million people), Spain (1.5 million people), Italy (2.6 million people), and France (2.6 million people) in those people > 45 years of age. CONCLUSIONS: Smoking rates appear to provide a useful method of estimating current COPD prevalence in those countries where more objective data are unavailable. These results are important because recognition of the true burden of disease and corresponding efforts to increase early identification of COPD can help to reduce the morbidity and mortality associated with COPD in populations at risk.

Conclusion. Lessons from the novel D2 dopamine receptor, beta2-adrenoceptor agonist, Viozan: chronic obstructive pulmonary disease and drug development implications.

The development of novel drugs for the treatment of chronic obstructive pulmonary disease (COPD) poses significant challenges. The mechanisms through which the chronic symptoms of COPD arise are poorly understood, making identification of potential therapeutic targets and in vivo evaluation of potential therapies extremely difficult. Despite these challenges, a unique approach of combined D2 dopamine, beta2-adrenoceptor agonism was identified as a valid potential target for the treatment of key COPD symptoms, the therapeutic potential of which was investigated in a series of preclinical evaluations. Subsequent clinical assessment has amassed a wealth of data from over 4000 patients, providing valuable insights into COPD, clinical trial design and the value of patient self-assessment tools.

Symptoms are an important outcome in chronic obstructive pulmonary disease clinical trials: results of a 3-month comparative study using the Breathlessness, Cough and Sputum Scale (BCSS).

The need to manage the key symptoms of chronic obstructive pulmonary disease (COPD) (breathlessness, cough and sputum) is an important treatment objective. Viozan (sibenadet HCl, AR-C68397AA) is a novel dual D2 dopamine receptor, beta2-adrenoceptor agonist, which combines conventional bronchodilatory activity with the sensory nerve modulation afforded by dopamine agonism. The efficacy of this agent in relieving patient symptoms has been determined in a series of large-scale clinical studies; the results of a 3-month, placebo-controlled multi-centre study are reported. Effect on patient symptoms was determined using a novel patient-reported assessment instrument, the Breathlessness, Cough and Sputum Scale (BCSS). Patients with smoking-related COPD were required to complete a 2-week baseline period before being randomized to one of three treatment groups; sibenadet (500 microg three times daily) plus placebo (twice daily); salmeterol (50 microg twice daily) plus placebo (three times daily); placebo (twice daily) plus a second placebo (three times daily). All treatments were delivered via pressurized metered dose inhaler (pMDI) for 12 weeks. From enrolment, patients were required to complete daily diary cards to record symptoms of breathlessness, cough and sputum, medication use and adverse events. The primary outcome measure was the difference between the mean BCSS total score measured over the baseline period and the mean BCSS total score in the final 4 weeks of the treatment period. Secondary measures included assessment of lung function, rescue medication use, exacerbations, health-related quality of life, opinion of efficacy and safety. Although an initial reduction in BCSS total score (indicating symptom improvement) was seen with sibenadet therapy, this effect was not maintained for the study duration. Salmeterol therapy, however, resulted in a sustained reduction in BCSS total score. No notable benefit over placebo was seen in lung function, exacerbations or health-related quality of life with either active treatment. While the results of this study failed to demonstrate sustained efficacy with sibenadet therapy, they do indicate the value of symptom assessment in the clinical evaluation of new drugs for the treatment of COPD.