COPD
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Randomized Controlled Trial Multicenter Study
Physiologic variables and functional status independently predict COPD hospitalizations and emergency department visits in patients with severe COPD.
Using clinical and claims records from the National Emphysema Treatment Trial, we sought to identify factors that accurately predicted COPD exacerbations. This prospective cohort study consisted of subjects with severe emphysema randomized to medical therapy. Exacerbations were defined as a hospitalization or emergency department visit for COPD. ⋯ In 610 participants, 26.6% had a COPD exacerbation over 1-year follow-up. In a model incorporating spirometry, PaO2, dyspnea, prior exacerbations and co-morbidity, a 5-point decrement in percent predicted FEV1 (OR 1.16, 95% CI 1.00-1.34) and a 5-point worsening in SOBQ (OR 1.08, 1.02-1.14) independently predicted exacerbations (AUC for full model 0.68). Combining physiologic variables, dyspnea, prior exacerbations and co-morbidity may be useful in identifying patients at high risk for COPD exacerbations.
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The purpose of this endeavor is to compare the morbidity, mortality and costs of LVRS versus transplantation in severe emphysema. This was a retrospective review of severe emphysema patients who received LVRS (n = 70) from 1994-1999, or transplant (n = 87) from 1994-2004. Change in functional status was calculated by the change in modified BODE (mBODE) score. ⋯ During a mean follow-up of 2.4 +/- 2.5 years after transplant and 5.0 +/- 3.1 years after LVRS, transplantation mean total costs were greater ($381,732 vs. $140,637, p < 0.0001). Transplantation patients spent more time in the hospital (74.3 +/- 81.3 vs. 39.5 +/- 66.7 days, p = 0.009) and had more outpatient visits (29.9 +/- 28.8 vs. 12.3 +/- 12.6 visits, p < 0.0001). In patients who survive over 1 year, transplantation provides a higher level of functional status and a greater improvement in airflow obstruction, dyspnea, exercise tolerance, and mBODE score, but costs more and carries greater mortality.
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Multicenter Study
Decline in FEV1 in relation to incident chronic obstructive pulmonary disease in a cohort with respiratory symptoms.
Data on the relationship between decline in lung function and development of COPD are sparse. We assessed the decline in FEV1 during 10 years among subjects with respiratory symptoms by two different methods and evaluated risk factors for decline and its relation to incident Chronic Obstructive Pulmonary Disease, COPD. A cross-sectional postal questionnaire was in 1986 sent to 6610 subjects of three age strata. ⋯ Gender-specific analysis revealed that smoking was a stronger risk factor in women than in men, while higher age was a significant risk factor in men only. In conclusion, decline in FEV1 was associated with age, smoking, and chronic productive cough, but the risk factor pattern was gender-dependent. Among incident cases of COPD the decline was steeper and close to a quarter had a rapid decline.
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Review
Assessment of the economic burden of COPD in the U.S.: a review and synthesis of the literature.
The costs of chronic obstructive pulmonary disease (COPD) pose a major economic burden to the United States. Studies evaluating COPD costs have generated widely variable estimates; we summarized and critically compared recent estimates of the annual national and per-patient costs of COPD in the U. S. ⋯ Studies of both national and per-patient costs that use data approximately 8-10 years old or older have produced estimates that tend to deviate from these ranges. Cost-of-illness studies using recent data underscore the substantial current cost burden of COPD in the U. S.
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Increased bronchial epithelial cell apoptosis and CD8+ T-cell numbers in the blood and airways have been reported in COPD. These cells can induce apoptosis via the granzyme-b/perforin-mediated pathway. We hypothesized that increased levels of granzyme-b/perforin would be detected in COPD, contributing to apoptosis and tissue damage. ⋯ Most circulating NK cells expressed granzyme-b/perforin, with the median fluorescence intensity of staining increased in both COPD groups and asymptomatic smokers. Granzyme-mediated apoptosis may thus be one mechanism of lung injury in COPD. The changes that persist despite smoking cessation in COPD likely reflect pathophysiological changes in COPD as opposed to the effects of smoking per se.