Despite the considerable progress in the classification of the idiopathic interstitial pneumonias (IIPs), the lack of an international standard has resulted in variable and confusing diagnostic criteria and terminology. The advent of high-resolution computerized tomography, the narrowed pathologic definition of usual interstitial pneumonia (UIP) and recognition of the prognostic importance of separating UIP from other IIP patterns have profoundly changed the approach to the IIPs. This is an international Consensus Statement defining the clinical manifestations, pathology, and radiologic features of patients with IIP. The major objectives of this statement are to standardize the classification of the idiopathic interstitial pneumonias (IIPs) and to establish a uniform set of definitions and criteria for the diagnosis of IIPs. The targeted specialties are pulmonologists, radiologists, and pathologists. A multidisciplinary core panel was responsible for review of background articles and writing of the document. In addition, this group reviewed the clinical, radiologic, and pathologic aspects of a wide spectrum of cases of diffuse parenchymal interstitial lung diseases to establish a uniform and consistent approach to these diseases and to clarify the terminology, definitions, and descriptions used in routine clinical practice. The final statement was drafted after a series of meetings of the entire committee. The level of evidence for the recommendations made in this statement is largely that of expert opinion developed by consensus. This classification of IIPs includes seven clinico-radiologic-pathologic entities: idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia, cryptogenic organizing pneumonia, acute interstitial pneumonia, respiratory bronchiolitis-associated interstitial lung disease, desquamative interstitial pneumonia, and lymphoid interstitial pneumonia. The need for dynamic interaction between pathologists, radiologists, and pulmonologists to accurately diagnose these disorders is emphasized. The level of evidence for the recommendations made in this Statement is largely that of expert opinion developed by consensus. This Statement is an integrated clinical, radiologic, and pathologic approach to the classification of the IIPs. Use of this international multidisciplinary classification will provide a standardized nomenclature and diagnostic criteria for IIP. This Statement provides a framework for the future study of these entities. Key Messages * Unclassifiable interstitial pneumonia : Some cases are unclassifiable for a variety of reasons (see text). † This group represents a heterogeneous group with poorly characterized clinical and radiologic features that needs further study. ‡ COP is the preferred term, but it is synonymous with idiopathic bronchiolitis obliterans organizing pneumonia.
The efficacy and safety of budesonide/formoterol in a single inhaler compared with placebo, budesonide and formoterol were evaluated in patients with moderate-to-severe chronic obstructive pulmonary disease (COPD).In a 12-month, randomised, double-blind, placebo-controlled, parallel-group study in 812 adults (mean age 64 yrs, mean forced expiratory volume in one second (FEV1) 36% predicted normal), patients received two inhalations twice daily of either budesonide/ formoterol (Symbicort1) 160/4.5 mg (delivered dose), budesonide 200 mg (metered dose), formoterol 4.5 mg or placebo. Severe exacerbations and FEV1 (primary variables), peak expiratory flow (PEF), COPD symptoms, health-related quality of life (HRQL), mild exacerbations, use of reliever b 2 -agonist and safety variables were recorded.Budesonide/formoterol reduced the mean number of severe exacerbations per patient per year by 24% versus placebo and 23% versus formoterol. FEV1 increased by 15% versus placebo and 9% versus budesonide. Morning PEF improved significantly on day 1 versus placebo and budesonide; after 1 week, morning PEF was improved versus placebo, budesonide and formoterol. Improvements in morning and evening PEF versus comparators were maintained over 12 months. Budesonide/formoterol decreased all symptom scores and use of reliever b 2 -agonists significantly versus placebo and budesonide, and improved HRQL versus placebo. All treatments were well tolerated.These results suggest a role for budesonide/formoterol in the long-term management of moderate-to-severe chronic obstructive pulmonary disease. Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death in the world [1], with increasing prevalence and mortality predicted in the coming decades [2]. COPD is a serious and disabling disease, which imposes a large burden on patients, healthcare systems and society.In patients with COPD, lung function deteriorates progressively over several years with increasing symptoms (e.g. dyspnoea, chest tightness, cough and sputum production); acute exacerbations are common, particularly in later stages, and these have considerable impact on patients9 daily activities and well-being [3]. Cigarette smoking is the major aetiological factor in COPD and smoking cessation is the only factor which has been shown to influence the decline in forced expiratory volume in one second (FEV1) [4,5]. However, the COPD-related inflammatory process in the airways initiated by smoking persists after cessation of smoking [6], and effective treatment is needed in past smokers with COPD [7].The pharmacotherapy of COPD largely consists of mucolytics, bronchodilators, such as b 2 -agonists, anticholinergics, theophylline and anti-inflammatory drugs i.e. inhaled corticosteroids, often taken in combination [2]. Consequently, there is a need for better treatment options to relieve symptoms, reduce exacerbations and to provide better health-related quality of life (HRQL) for individual patients. The long-acting b 2 -agonists formoterol a...
Women cooking with biomass fuels have increased respiratory symptoms and a slight average reduction in lung function compared with those cooking with gas.
We hypothesised that biomass smoke exposure is associated with an airway-predominant chronic obstructive pulmonary disease (COPD) phenotype, while tobacco-related COPD is associated with an emphysema-predominant phenotype.In this cross-sectional study, female never-smokers with COPD and biomass exposure (n521) and female ex-cigarette smokers with COPD without biomass exposure (n522) completed computed tomography (CT) at inspiration and expiration, pulmonary function, blood gas, exercise tolerance, and quality of life measures. Two radiologists scored the extent of emphysema and air trapping on CT. Quantitative emphysema severity and distribution and airway wall thickness were calculated using specialised software.Women in the tobacco group had significantly more emphysema than the biomass group (radiologist score 2.3 versus 0.7, p50.001; emphysema on CT 27% versus 19%, p50.046; and a larger size of emphysematous spaces, p50.006). Women in the biomass group had significantly more air trapping than the tobacco group (radiologist score 2.6 and 1.5, respectively; p50.02) and also scored lower on the symptom, activities and confidence domains of the quality of life assessment and had lower oxygen saturation at rest and during exercise (p,0.05).Biomass smoke exposure is associated with less emphysema but more air trapping than tobacco smoke exposure, suggesting an airway-predominant phenotype. @ERSpublications Biomass smoke causes less emphysema but more air trapping than tobacco smoke: airwaypredominant COPD phenotype?
Women exposed domestically to biomass develop chronic obstructive pulmonary disease with clinical characteristics, quality of life, and increased mortality similar in degree to that of tobacco smokers.
A case-control study was performed in women older than 40 yr of age to evaluate the risk of cooking with traditional wood stoves for chronic bronchitis and chronic airway obstruction (CAO). The subjects were recruited from patients attending a referral chest hospital in Mexico City. We selected 127 patients with chronic bronchitis or CAO, of which 63 had chronic bronchitis alone, 23 had CAO alone (FEV1 less than 75% of predicted), and 41 had both chronic bronchitis and CAO (cases). Four control groups were selected: 83 patients with pulmonary tuberculosis, 100 patients with interstitial lung diseases, 97 patients with ear, nose and throat ailments, and 95 healthy visitors to the hospital (controls). Exposure to wood smoke, assessed as any or none, and as hour-years (years of exposure multiplied by average hours of exposure per day) was significantly higher in cases than in controls. Crude odds ratios for wood smoke exposure were 3.9 (95% CI, 2.0 to 7.6) for chronic bronchitis only, 9.7 (95% CI, 3.7 to 27) for CAO plus chronic bronchitis, and 1.8 (95% CI, 0.7 to 4.7) for CAO only. Differences in exposure to wood smoke persisted after adjusting by stratification and logistic regression for age, income, education, smoking, place of residence, and place of birth. Risk of chronic bronchitis alone and chronic bronchitis with CAO increased linearly with hour-years of cooking with a wood stove; odds ratios for exposure to more than 200 hour-years compared with nonexposed were 15.0 (95% CI, 5.6 to 40) for chronic bronchitis only and 75 (95% CI, 18 to 306) for chronic bronchitis with CAO. The findings support a causal role of domestic wood smoke exposure in chronic bronchitis and chronic airflow obstruction.
The health and safety claims regarding electronic nicotine delivery devices should be subject to evidentiary review. The potential benefits of electronic cigarettes to an individual smoker should be weighed against potential harm to the population of increased social acceptability of smoking and use of nicotine, the latter of which has addictive power and untoward effects. As a precaution, electronic nicotine delivery devices should be restricted or banned until more information about their safety is available. If they are allowed, they should be closely regulated as medicines or tobacco products.
The clinical course of chronic pigeon breeder's lung (CPBL) is unknown, especially in comparison with usual interstitial pneumonia (UIP). We studied a cohort of 125 consecutive patients with interstitial lung diseases, including 78 patients with CPBL (74 biopsied) and 47 patients with UIP in the lung biopsy. Patients with UIP were divided into 17 without bird exposure (UIP) and 30 with bird exposure (UIP + BE). All patients were treated with corticosteroids and followed for 33 +/- 23 months. The best predictors of mortality (Cox proportional hazards model) were age > 44 yr, with a relative risk (RR) of 2.5 and 95% confidence interval (CI) of 1.4 to 4.7, masculine gender (RR 4.0, CI 2.1 to 7.6), x-ray honeycombing (RR 7.0, CI 3.8 to 12.7), and severity of fibrosis in the lung biopsy (RR 4.8, CI 2.3 to 9.7). Survival in CPBL 5 yr after diagnosis was 0.71 (SEM 0.08) and in UIP was 0.23 (SEM 0.08), with no statistical difference between UIP + BE and UIP. After adjusting for severity of fibrosis and honeycombing, however, the correlation of diagnosis with survival disappeared. In conclusion, mortality in CPBL is considerable, but lower than in UIP. Lung fibrosis and honeycombing seem to be a final common pathway for the ILD. Adjusting for them, the effect of diagnosis in survival is not significant.
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