COPD
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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.
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The objective of this study was to evaluate the definitions for classification of chronic obstructive pulmonary disease (COPD) recommended by the American Thoracic Society (ATS) and the Global Initiative for Chronic Obstructive Lung Disease (GOLD). Using data from the U. S. population-based third National Health and Nutrition Examination Survey (NHANES III), we compared the number of individuals in the U. ⋯ Based on our estimation, approximately 0.9 million (26%) of symptomatic individuals out of the 3.6 million U. S. adults aged 20-49 years who have airflow obstruction (FEV1/FVC < LLN and FEV1 < LLN definition) may have undiagnosed respiratory disease. In conclusion, using the FEV1/FVC < 0.70 criterion will substantially under-diagnose airway obstruction in younger individuals and substantially over-diagnose COPD in older individuals.
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Inflammatory lung diseases are characterised by increased expression of multiple inflammatory genes that are regulated by proinflammatory transcription factors, such as NF-kappaB. Gene expression is regulated by modifications such as acetylation of core histones through the concerted action of coactivators such as CBP (cAMP-response element binding protein (CREB)-binding protein) which have intrinsic histone acetyltransferase (HAT) activity and are able to recruit other HAT enzymes. Conversely gene repression is mediated via histone deacetylases (HDAC) and other corepressors. ⋯ Similar mechanisms may also account for the steroid resistance seen within latent adenovirus infections. The reduction in HDAC activity induced by oxidative stress can be restored by theophylline, acting through specific kinases, which may be able to reverse steroid resistance in COPD and other inflammatory lung diseases. The modulation of HAT/HDAC activity may lead to the development of novel anti-inflammatory approaches to inflammatory lung diseases that are currently difficult to treat.
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Chronic obstructive pulmonary disease (COPD) is a costly cause of morbidity and mortality in the U. S. The objective of this study was to use contemporary national data-specifically, those from the 2000 Medical Expenditure Panel Survey (MEPS)-to estimate direct costs of COPD in the U. ⋯ Mean attributable costs per patient were estimated at dollar 2,507, with more than one-half of these costs (dollar 1,365) associated with hospitalization. Mean excess costs of COPD, after adjustment for sociodemographic factors and smoking status, were substantially higher, at dollar 4,932 per patient. Results of our study indicate that COPD-associated healthcare utilization and expenditures are considerable, and that annual per-patient costs of COPD are comparable to those of other chronic diseases of the middle-aged and elderly.
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Models of emphysema produced by exposing animals to cigarette smoke (CS) have potential for use in testing treatments of this disease. To better characterize development of emphysema in an animal model, male and female mice of the B6C3F1 and A/J strains were exposed to CS at 250 mg total particulate material (TPM)/m3 for 15 weeks. Emphysema was evident in both strains of mice to differing degrees of severity. ⋯ Neither the injections nor inhalation exposures of ATRA in either strain of mouse caused reversal of the emphysema. In summary, CS-induced emphysema was more severe in A/J mice than in B6C3F1 mice. Treatment with ATRA did not reverse emphysema in either strain of CS-exposed mice.