Annals of the American Thoracic Society
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The aim of bronchial thermoplasty is to improve asthma symptoms by reducing central airway smooth muscle mass. Up to now, the reduction of smooth muscle mass has been documented for only 1 group of 10 patients who had 15% or more of their pretreatment total bronchial biopsy area occupied by smooth muscle. ⋯ For patients with severe asthma, bronchial thermoplasty reduced the smooth muscle mass of treated airway segments, regardless of the baseline level of muscle mass. Treatment also altered the deposition of collagen. At follow-up, bronchial thermoplasty improved asthma control; however, the limited number of subjects did not allow us to evaluate possible correlations between these improvements and the studied histological parameters. Further studies are needed to confirm these results and evaluate their persistence.
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Review Meta Analysis
A Comprehensive Analysis of the Impact of Pseudomonas aeruginosa Colonization on Prognosis in Adult Bronchiectasis.
Eradication and suppression of Pseudomonas aeruginosa is a key priority in national guidelines for bronchiectasis and is a major focus of drug development and clinical trials. An accurate estimation of the clinical impact of P. aeruginosa in bronchiectasis is therefore essential. ⋯ P. aeruginosa is associated with an approximately threefold increased risk of death and an increase in hospital admissions and exacerbations in adult bronchiectasis.
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Sepsis contributes to one in every two to three inpatient hospital deaths. Early recognition and treatment are instrumental in reducing mortality, yet there are substantial quality gaps. Sepsis bundles containing quality metrics are often used in efforts to improve outcomes. Several prominent organizations have published their own bundles, but there are few head-to-head comparisons of content. ⋯ There is a lack of consensus on component elements and timing goals across highly recognized sepsis bundles. These differences highlight an urgent need for comparative effectiveness research to guide future implementation and for metrics to evaluate progress. None of the widely instituted bundles include metrics to evaluate sepsis recognition or diagnostic accuracy.
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Allergy and viral respiratory infections have long been recognized as two of the most important risk factors for exacerbations of asthma. These observations have raised questions regarding potential interactions between these two important risk factors. For example, does allergy diminish the antiviral response, thereby promoting exacerbations of asthma? Alternately, do viral respiratory infections potentiate ongoing allergic inflammation in the airway? The answers to these questions are likely to have implications regarding the prevention and treatment of exacerbations of asthma. This article reviews that clinical evidence linking viral infections and allergy to exacerbations of asthma, reviews potential interactions between these two risk factors, and discusses possible application of new insights in virus/allergen interactions to the prevention and treatment of exacerbations of asthma.
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Asthma exacerbations are an important cause of asthma morbidity. Although viral infection of the upper airway is a common cause of asthma exacerbations, the reasons why some patients with asthma are exacerbation prone and others are exacerbation resistant are not fully understood. In this review, we examine whether Type 2 inflammation modifies airway function to make patients more susceptible to asthma exacerbations. ⋯ These trials include studies with omalizumab (an inhibitor of IgE) and others with inhibitors of Type 2 cytokines (IL-4, IL-5, and IL-13). All of these trials consistently show that inhibiting the Type 2 pathway causes a clinically significant reduction in asthma exacerbations. Thus, it is now clear that Type 2 inflammation is an important mechanism of susceptibility to asthma exacerbation.