Chest
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Randomized Controlled Trial
Lung Function in Rural Guatemalan Women Before and After a Chimney Stove Intervention to Reduce Woodsmoke Exposure: Results From RESPIRE and CRECER.
COPD is the third most frequent cause of death globally, with much of this burden attributable to household biomass smoke exposure in developing countries. As biomass smoke exposure is also associated with cardiovascular disease, lower respiratory infection, lung cancer, and cataracts, it presents an important target for public health intervention. ⋯ In these young Guatemalan women, there was no association between lung function and early randomization to a chimney stove or personal wood smoke exposure. Future stove intervention trials should incorporate cleaner stoves, longer follow-up, or potentially susceptible groups to identify meaningful differences in lung function.
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Multicenter Study
Blastomycosis in Indiana: Clinical and Epidemiologic Patterns of Disease Gleaned from a Multicenter Retrospective Study.
To better understand clinical and epidemiologic patterns of blastomycosis, we report on a large series of blastomycosis in Indiana. ⋯ The incidence of blastomycosis in Central Indiana may be on the rise. Physicians in endemic areas should be aware of the potentially fulminant consequences of the disease.
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Smoking-induced lung diseases were extremely rare prior to the 20th century. With commercialization and introduction of machine-made cigarettes, worldwide use skyrocketed and several new pulmonary diseases have been recognized. The majority of pulmonary diseases caused by cigarette smoke (CS) are inflammatory in origin. ⋯ We review here the known cellular and molecular mechanisms of CS-induced diseases, including COPD, respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia, acute eosinophilic pneumonia, chronic rhinosinusitis, pulmonary Langerhans cell histiocytosis, and chronic bacterial infections. We also discuss inflammation induced by secondhand and thirdhand smoke exposure and the pulmonary diseases that result. New targeted antiinflammatory therapeutic options are currently under investigation and hopefully will yield promising results for the treatment of these highly prevalent smoking-induced diseases.
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Pathophysiologic gaps in the actions of currently available treatments for asthma and COPD include neutrophilic inflammation, airway remodeling, and alveolar destruction. All of these processes can be modulated by cyclic adenosine monophosphate-elevating prostaglandins E2 and I2 (also known as prostacyclin). These prostanoids have long been known to elicit bronchodilation and to protect against bronchoconstriction provoked by a variety of stimuli. ⋯ By contrast, excessive prostanoid production and signaling might contribute to both the increased susceptibility to infections that drive COPD exacerbations and the inadequate alveolar repair that characterizes emphysema. Inhibition of endogenous prostanoid synthesis or signaling, thus, has therapeutic potential for these types of patients. By virtue of their pleiotropic capacity to modulate numerous pathophysiologic processes relevant to the expression and natural history of airway diseases, prostanoids emerge as attractive targets for therapeutic manipulation.
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Multicenter Study
Discontinuation of inhaled corticosteroids in COPD and the risk reduction of pneumonia.
The widespread use of inhaled corticosteroids (ICSs) for COPD treatment has been questioned. Recent studies of weaning some patients with COPD off ICSs found little or no adverse consequences compared with long-acting bronchodilators. It is unclear, however, whether discontinuation of ICSs reduces the elevated risk of pneumonia associated with these drugs. ⋯ Discontinuation of ICS use in COPD is associated with a reduction in the elevated risk of serious pneumonia, particularly so with fluticasone.