Chronic Obstructive Pulmonary Disease Status Research Articles

Clinical characteristics and outcomes of hospitalized heart failure patients with systolic dysfunction and chronic obstructive pulmonary disease: findings from OPTIMIZE‐HF

Chronic obstructive pulmonary disease (COPD) is common in heart failure (HF) patients, yet the population is poorly characterized and associated with conflicting outcomes data. We aimed to evaluate the clinical characteristics and outcomes of HF patients with systolic dysfunction and COPD in a large acute HF registry. OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) was a performance-improvement registry of patients hospitalized with HF (n =48 612), which included a pre-specified subgroup of patients (n =5,701) with 60- to 90-day follow-up. We performed a retrospective analysis of the clinical characteristics and outcomes (length of stay, and in-hospital and 60-day mortality) of patients with systolic dysfunction according to baseline COPD status. COPD was present in 25% of the patients. These patients had more co-morbidities compared with patients without COPD. They were less likely to receive a beta-blocker or angiotensin-converting enzyme inhibitor during hospitalization and at discharge (P < 0.001). COPD was associated with an increased median length of stay [5 days (interquartile range 3-8) vs. 4 days (interquartile range 3-7), P < 0.0001] and increased in-hospital all-cause and non-cardiovascular (CV) mortality, with rates of 4.5% vs. 3.7% (P =0.01) and 1.0% vs. 0.6% (P =0.01), respectively, for the two endpoints, but similar 60-day mortality (6.2% vs. 6.0%, P =0.28). After risk adjustment, the in-hospital non-CV mortality remained increased (odds ratio 1.65, 95% confidence interval 1.12-2.41; P =0.01). The presence of COPD in HF patients with systolic dysfunction is associated with an increased burden of co-morbidities, lower use of evidence-based HF medications, longer hospitalizations, and increased in-hospital non-CV mortality, but similar post-discharge mortality.

Obstructive airway disease and edentulism in the atherosclerosis risk in communities (ARIC) study

ObjectivesWe examined the potential association between prior chronic obstructive pulmonary disease (COPD) and edentulism, and whether the association varied by COPD severity using data from the Dental Atherosclerosis Risk in...

Clinical applications of gene-based risk prediction for lung cancer and the central role of chronic obstructive pulmonary disease.

Lung cancer is the leading cause of cancer death worldwide and nearly 90% of cases are attributable to smoking. Quitting smoking and early diagnosis of lung cancer, through computed tomographic screening, are the only ways to reduce mortality from lung cancer. Recent epidemiological studies show that risk prediction for lung cancer is optimized by using multivariate risk models that include age, smoking exposure, history of chronic obstructive pulmonary disease (COPD), family history of lung cancer, and body mass index. It has also been shown that COPD predates lung cancer in 65–70% of cases, conferring a four- to sixfold greater risk of lung cancer compared to smokers with normal lung function. Genome-wide association studies of smokers have identified a number of genetic variants associated with COPD or lung cancer. In a case–control study, where smokers with normal lungs were compared to smokers who had spirometry-defined COPD or histology confirmed lung cancer, several of these variants were shown to overlap, conferring the same susceptibility or protective effects on both COPD and lung cancer (independent of COPD status). In this perspective article, we show how combining clinical data with genetic variants can help identify heavy smokers at the greatest risk of lung cancer. Using this approach, we found that gene-based risk testing helped engage smokers in risk mitigating activities like quitting smoking and undertaking lung cancer screening. We suggest that such an approach could facilitate the targeted selection of smokers for cost-effective life-saving interventions.

Quantitative Computed Tomography in COPD: Possibilities and Limitations

Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease that is characterized by chronic airflow limitation. Unraveling of this heterogeneity is challenging but important, because it might enable more accurate diagnosis and treatment. Because spirometry cannot distinguish between the different contributing pathways of airflow limitation, and visual scoring is time-consuming and prone to observer variability, other techniques are sought to start this phenotyping process. Quantitative computed tomography (CT) is a promising technique, because current CT technology is able to quantify emphysema, air trapping, and large airway wall dimensions. This review focuses on CT quantification techniques of COPD disease components and their current status and role in phenotyping COPD.

Does 18F-FDG Uptake by Respiratory Muscles on PET/CT Correlate with Chronic Obstructive Pulmonary Disease?

(18)F-FDG muscle uptake is evident in some benign physiologic processes as seen in the respiratory muscles of patients with chronic obstructive pulmonary disease (COPD) and labored breathing. The purpose of this study was to correlate the presence of COPD with the patterns of (18)F-FDG uptake by muscles as demonstrated by PET/CT scans. (18)F-FDG PET/CT scans and pulmonary function tests (PFTs) were performed for 63 consecutive patients with newly diagnosed or highly suspected lung cancer. Presurgical pulmonary function tests by way of spirometry examinations were performed as the standard of care. Patients were grouped into those with normal spirometry findings and those with mild to very severe COPD. The guidelines of the Global Initiative for Chronic Obstructive Lung Disease were used for staging COPD and obstructive impairment. A nuclear medicine physician and 2 residents who did not know the COPD status retrospectively reviewed PET/CT scans and kept a log for cases of increased (18)F-FDG uptake in the respiratory muscles (diaphragm, intercostal muscles, and scalene muscles). The χ(2) test and Cramer V were used to evaluate the correlation between increased (18)F-FDG uptake by muscles and the presence of COPD. Sixty-three patients underwent both (18)F-FDG PET/CT and PFT within 1 mo of each another without interval therapy. Of the 63 patients, 26 (41%) had no spirometric obstruction and 37 (59%) had spirometric obstruction. Of these, 30 (81%) had a previously established diagnosis of COPD (1 mild, 26 moderate, 9 severe, and 1 very severe). Excessive (18)F-FDG uptake was seen in at least 2 of the 3 muscles (diaphragm and intercostal muscles) in 27 (73%) of the 37 patients with COPD and obstructive ventilatory impairment. The severity of COPD and obstruction showed a significant correlation with the presence of abnormal (18)F-FDG uptake by any of the 3 muscle types, particularly when 2 groups of muscles were involved (Cramer V = 0.60, χ(2) P < 0.001). Our study revealed a strong correlation between increased (18)F-FDG uptake by respiratory muscles and the presence of COPD.

Atherosclerotic plaques in the internal carotid artery and associations with lung function assessed by different methods

Previous studies on associations between reduced lung function and cardiovascular disease (CVD) have mainly been based on forced expiratory volume in 1-s (FEV(1) ) and vital capacity (VC). This study examined potential associations between five different lung function variables and plaques in the internal carotid artery (ICA). Subjects (n = 450) from a previous population-based respiratory questionnaire survey [current smokers without lower respiratory symptoms, subjects with a self-reported diagnosis of chronic obstructive pulmonary disease (COPD) and never-smokers without lower respiratory symptoms] were examined using spirometry, body plethysmography and measurements of diffusing capacity for CO (D(L,CO) ). Plaques in the ICA were assessed by ultrasonography. Two hundred and twenty subjects were current smokers, 139 ex-smokers and 89 never-smokers. COPD was diagnosed in 130 subjects (GOLD criteria). Plaques in the ICA were present in 231 subjects (52%). General linear analysis with adjustment for established risk factors for atherosclerosis, including C-reactive protein, showed that D(L,CO) was lower [77.4% versus 83.7% of predicted normal (PN), P = 0.014] and residual volume (RV) was higher (110.3% versus 104.8% of PN, P = 0.020) in subjects with than without plaques in the ICA. This analysis did not show any statistically significant association between plaques and FEV(1) or VC. The occurrence of plaques in the ICA was associated with low D(L,CO) and high RV, but not significantly with FEV(1) or COPD status. The results suggest that the relationships between reduced lung function, COPD and CVD are complex and not only linked to bronchial obstruction and low-grade systemic inflammation.

Elevated placenta growth factor predicts pneumonia in patients with chronic obstructive pulmonary disease under inhaled corticosteroids therapy

BackgroundAn increased incidence of pneumonia in patients with chronic obstructive pulmonary disease (COPD) under inhaled corticosteroid (ICS) therapy was noticed in previous studies. We performed a prospective study to elucidate the risk factors for the development of pneumonia in this group of patients.MethodsA prospective, non-randomized study with patients diagnosed as having COPD from 2007 to 2008 identified in the Far Eastern Memorial Hospital were recruited. We recorded data for all patients, including clinical features and signs, demographic data, lung function status, and medications. Bio-markers such as C-reactive protein (CRP) and placenta growth factor (PlGF) were checked at first diagnosis. Every acute exacerbation was also recorded, especially pneumonia events, which were confirmed by chest radiography. Multivariate analysis was performed with stepwise logistic regression for pneumonia risk factors.Results274 patients were diagnosed as having COPD during the study period and 29 patients suffered from pneumonia with a prevalence of 10.6%. The rate was significantly higher in patients with ICS therapy (20/125, 16%) compared with those without ICS (9/149, 6%) (p = 0.02). We stratified ICS therapy into medium dose (500-999 ug/day fluticasone equivalent, 71 patients) and high dose (1000 ug/day and higher fluticasone equivalent, 54 patients) group. There was no statistical difference in the incidence of pneumonia between these two group (medium dose: 13/71, 18.3% vs. high dose: 7/54, 12.9%, p = 0.47). Multivariate analysis was performed to identify the risk factors for developing pneumonia and included forced expiratory volume in one second (FEV1) less than 40% of predicted (odds ratio (OR) 2.2, 95% confidence interval (CI): 1.1-6.9), ICS prescription ((OR) 2.4, 95% (CI): 1.3-8.7), the presence of diabetes mellitus (DM) (OR 2.6, 95% CI: 1.2-9.4) and PlGF level over 40 pg/L (OR 4.1, 95% CI: 1.5-9.9).ConclusionICS therapy in patients with COPD increased the risk of pneumonia. However, there was no relationship between the incidence of pneumonia and dosage of ICS. Additionally, advanced COPD status, DM and elevated PlGF level were independent risk factors for the development of pneumonia. PlGF would be a good novel biomarker for predicting pneumonia.

Total desmosines in plasma and urine correlate with lung function

The aim of the present study was to evaluate the relationship between the matrix degradation biomarkers, desmosine and isodesmosine (desmosines), and lung function. Plasma and creatinine-corrected urinary total desmosines (P- and U-desmosines, respectively), lung function and diffusing capacity of the lung for carbon monoxide (D(L,CO)) were measured in a cohort of subjects from the Swedish Twin Registry. Concentrations of U- and P-desmosines were measured in 349 and 318 subjects, respectively; approximately one-third of subjects had chronic obstructive pulmonary disease (COPD). Age, female sex, body mass index (BMI) and smoking were significantly associated with U-desmosines in a multiple linear regression analysis. In the overall population, after adjustments for age, sex, height, BMI and smoking, concentrations of U-desmosines were significantly correlated with all lung function measures, and P-desmosines with forced expiratory volume in 1 s and D(L,CO) (p<0.05). With the exception of residual volume versus P-desmosines, relationships between concentrations of desmosines and lung function measures were markedly stronger in subjects with COPD compared with those without COPD. These cross-sectional data showing associations between desmosines and several lung function variables suggest that desmosines, particularly U-desmosines, could be a useful biomarker of COPD status.

P2-106 Screening of lung function disorders among smokers in primary healthcare: A Russian Study

IntroductionSmoking is the main risk factor for chronic obstructive pulmonary disease (COPD). The prevalence of smoking in Russian Federation is one of the highest in the world. Many cases of...

Prevalence of COPD and its association with socioeconomic status in China: Findings from China Chronic Disease Risk Factor Surveillance 2007

BackgroundSocioeconomic status is likely an independent risk factor for Chronic Obstructive Pulmonary Disease (COPD), but little research has been done in China to study this association in a nationwide sample.MethodsWe used data from the 2007 China Chronic Disease Risk Factor Surveillance of 49,363 Chinese men and women aged 15-69 years to examine the association between the prevalence of self-reported physician diagnosed COPD and socioeconomic status defined by both educational level and annual household income. Multivariable logistic regression modelling was performed with adjustement for potential confounders.ResultsBoth low educational attainment and low household income were independently associated with higher risk of physician-diagnosed COPD. Compared to subjects with high educational level, subjects with low educational level had a significantly increased risk of COPD (OR 1.67, 95%CI 1.32-2.13, p for trend< 0.001 for urban, OR 1.76, 95%CI 1.34-2.30, p for trend < 0.001 for rural) after adjusting for age, sex, smoking status, passive smoking and geographic regions. Similarly increased risk was observed for household income and COPD in urban (OR 1.64, 95%CI 1.28-2.09, P for trend< 0.001) but not rural areas. Among never smokers, low educational level and household income were still associated with a significant higher prevalence of COPD (OR 1.77, 95%CI 1.40-2.25, OR 1.31, 95%CI 1.05-1.62). Removal of those with asthma diagnosis did not alter the observed associations.ConclusionsSocioeconomic status is a risk factor for self-reported physician-diagnosed COPD independently of current or passive smoking. Prospective studies are needed in China to better understand the association between socioeconomic status and COPD.

The influence of smoking status on malnutrition risk and 1-year mortality in outpatients with chronic obstructive pulmonary disease

Introduction: Smoking status in outpatients with chronic obstructive pulmonary disease (COPD) has been associated with a low body mass index (BMI) and reduced mid-arm muscle circumference (Cochrane & Afolabi, 2004). Individuals with COPD identified as malnourished have also been found to be twice as likely to die within 1 year compared to non-malnourished patients (Collins et al., 2010). Although malnutrition is both preventable and treatable, it is not clear what influence current smoking status, another modifiable risk factor, has on malnutrition risk. The current study aimed to establish the influence of smoking status on malnutrition risk and 1-year mortality in outpatients with COPD. Methods: A prospective nutritional screening survey was carried out between July 2008 and May 2009 at a large teaching hospital (Southampton General Hospital) and a smaller community hospital within Hampshire (Lymington New Forest Hospital). In total, 424 outpatients with a diagnosis of COPD were routinely screened using the ‘Malnutrition Universal Screening Tool’, ‘MUST’ (Elia, 2003); 222 males, 202 females; mean (SD) age 73 (9.9) years; mean (SD) BMI 25.9 (6.4) kg m−2. Smoking status on the date of screening was obtained for 401 of the outpatients. Severity of COPD was assessed using the GOLD criteria, and social deprivation determined using the Index of Multiple Deprivation (Nobel et al., 2008). Results: The overall prevalence of malnutrition (medium + high risk) was 22%, with 32% of current smokers at risk (who accounted for 19% of the total COPD population). In comparison, 19% of nonsmokers and ex-smokers were likely to be malnourished [odds ratio, 1.965; 95% confidence interval (CI), 1.133–3.394; P = 0.015]. Smoking status remained an independent risk factor for malnutrition even after adjustment for age, social deprivation and disease-severity (odds ratio, 2.048; 95% CI, 1.085–3.866; P = 0.027) using binary logistic regression. After adjusting for age, disease severity, social deprivation, smoking status, malnutrition remained a significant predictor of 1-year mortality [odds ratio (medium + high risk versus low risk), 2.161; 95% CI, 1.021–4.573; P = 0.044], whereas smoking status did not (odds ratio for smokers versus ex-smokers + nonsmokers was 1.968; 95% CI, 0.788–4.913; P = 0.147). Table 1. Mean (SD) and percentage weight loss at 6 months and 1 year post-gastric band and gastric bypass Mean (SD) initial weight on admission for surgery (kg) Mean (SD) weight loss at 6 months (kg) Mean (SD) percentage total weight loss at 6 months Mean (SD) weight loss at 1 year (kg) Mean (SD) percentage total weight loss at 1 year LAGB 103.1 (7.0) 10.3 (7.7) 9.7* (6.9) 9.6 (8.6) 8.8* (7.7) LRYGB 133.6 (22.6) 30.1 (9.6) 22.1 (5.3) 41.7 (17.1) 29.7 (9.6) *P < 0.005 compared with LRYGB. Discussion: This study highlights the potential importance of combined nutritional support and smoking cessation in order to treat malnutrition. The close association between smoking status and malnutrition risk in COPD suggests that smoking is an important consideration in the nutritional management of malnourished COPD outpatients. Conclusions: Smoking status in COPD outpatients is a significant independent risk factor for malnutrition and a weaker (nonsignificant) predictor of 1-year mortality. Malnutrition significantly predicted 1 year mortality.

Epidemiology of Lung Cancer

Non-small cell lung cancer (NSCLC) and chronic obstructive pulmonary disease (COPD) have been proposed to have a mutual developmental mechanism, but their association has not been fully understood. We aimed to examine the association of the mutational landscape of NSCLC with co-morbid COPD.A total of 197 surgical specimens of early stage NSCLC were retrospectively collected from two independent sources, namely, the Japan Molecular Epidemiology for Lung Cancer Study and the Osaka City University Hospital cohort from 2010 to 2013. COPD and its severity were defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines and grading system. For molecular profiling of NSCLC patients with COPD, the extracted DNAs were deep-sequenced using next generation sequence technologies for somatic mutations in a maximum 72 cancer-associated genes. Logistic regression analysis was performed to evaluate the impact of COPD on the somatic mutations.The COPD group (n = 77), including 56 GOLD 1 and 21 GOLD 2 or 3 patients, had 58 squamous cell lung carcinoma (SCC) cases and 19 adenocarcinoma cases. The non-COPD group (n = 120) had 53 SCC cases, 64 adenocarcinoma cases, and three cases with other histology. The frequency of PIK3CA mutation was significantly higher in the COPD group than in the non-COPD group (10.4% vs. 1.7%, p = 0.015). Meanwhile, NFE2L2 mutation was observed only in SCC cases, with no difference in the frequency between the two groups (17.2% vs. 17.0%). In the multivariate logistic regression model with consideration for COPD status, age, smoking dose, pathological stage, and histology, significantly more PIK3CA mutation was observed in the presence of COPD (odds ratio = 5.31, 95% CI: 1.03–27.29, p = 0.046).PIK3CA mutation is a distinctive genetic feature of NSCLC with COPD, regardless of age, smoking dose, pathological stage, and histology.

Exhaled air molecular profiling in relation to inflammatory subtype and activity in COPD

Eosinophilic inflammation in chronic obstructive pulmonary disease (COPD) is predictive for responses to inhaled steroids. We hypothesised that the inflammatory subtype in mild and moderate COPD can be assessed by exhaled breath metabolomics. Exhaled compounds were analysed using gas chromatography and mass spectrometry (GC-MS) and electronic nose (eNose) in 28 COPD patients (12/16 Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I/II, respectively). Differential cell counts, eosinophil cationic protein (ECP) and myeloperoxidase (MPO) were measured in induced sputum. Relationships between exhaled compounds, eNose breathprints and sputum inflammatory markers were analysed and receiver operating characteristic (ROC) curves were constructed. Exhaled compounds were highly associated with sputum cell counts (eight compounds with eosinophils, 17 with neutrophils; p < 0.01). Only one compound (alkylated benzene) overlapped between eosinophilic and neutrophilic profiles. GC-MS and eNose breathprints were associated with markers of inflammatory activity in GOLD stage I (ECP: 19 compounds, p < 0.01; eNose breathprint r = 0.84, p = 0.002) (MPO: four compounds, p < 0.01; eNose r = 0.72, p = 0.008). ROC analysis for eNose showed high sensitivity and specificity for inflammatory activity in mild COPD (ECP: area under the curve (AUC) 1.00; MPO: AUC 0.96) but not for moderate COPD. Exhaled molecular profiles are closely associated with the type of inflammatory cell and their activation status in mild and moderate COPD. This suggests that breath analysis may be used for assessment and monitoring of airway inflammation in COPD.

The Association of Genome-Wide Significant Spirometric Loci with Chronic Obstructive Pulmonary Disease Susceptibility

Two recent metaanalyses of genome-wide association studies conducted by the CHARGE and SpiroMeta consortia identified novel loci yielding evidence of association at or near genome-wide significance (GWS) with FEV(1) and FEV(1)/FVC. We hypothesized that a subset of these markers would also be associated with chronic obstructive pulmonary disease (COPD) susceptibility. Thirty-two single-nucleotide polymorphisms (SNPs) in or near 17 genes in 11 previously identified GWS spirometric genomic regions were tested for association with COPD status in four COPD case-control study samples (NETT/NAS, the Norway case-control study, ECLIPSE, and the first 1,000 subjects in COPDGene; total sample size, 3,456 cases and 1,906 controls). In addition to testing the 32 spirometric GWS SNPs, we tested a dense panel of imputed HapMap2 SNP markers from the 17 genes located near the 32 GWS SNPs and in a set of 21 well studied COPD candidate genes. Of the previously identified GWS spirometric genomic regions, three loci harbored SNPs associated with COPD susceptibility at a 5% false discovery rate: the 4q24 locus including FLJ20184/INTS12/GSTCD/NPNT, the 6p21 locus including AGER and PPT2, and the 5q33 locus including ADAM19. In conclusion, markers previously associated at or near GWS with spirometric measures were tested for association with COPD status in data from four COPD case-control studies, and three loci showed evidence of association with COPD susceptibility at a 5% false discovery rate.

Ageing and long-term smoking affects KL-6 levels in the lung, induced sputum and plasma

BackgroundKL-6 is a high-molecular-weight glycoprotein classified as a human MUC1 mucin. It was hypothesized that KL-6 could be detectable in the circulating blood and especially in airway secretions in lung diseases associated with mucus production such as chronic obstructive pulmonary disease (COPD). Additional aims of this study were to investigate whether the levels of KL-6 in plasma and sputum are related to ageing and smoking history.MethodsThe concentrations of KL-6 in plasma and induced sputum supernatants from young and/or middle aged/elderly non-smokers, smokers and patients with COPD were assayed by ELISA (n = 201). The subjects were classified into five groups according to age, smoking status and presence of COPD. In addition, KL-6 expression in control and diseased lung i.e. samples from patients with COPD (n = 28), were analyzed by immunohistochemistry and digital image analysis.ResultsThe plasma levels of KL-6 increased with age both in non-smokers and smokers. Among middle aged/elderly subjects, plasma KL-6 levels in all smokers regardless of COPD were significantly higher than in non-smokers, whereas sputum levels of KL-6 were significantly higher in COPD compared not only to non-smokers but also to smokers. KL-6 was more prominently expressed in the bronchiolar/alveolar epithelium in COPD than in the control lungs. Plasma and sputum KL-6 levels correlated inversely with obstruction and positively with smoking history and ageing. The linear multiple regression analysis confirmed that age and cigarette smoking had independent effects on plasma KL-6.ConclusionsKL-6 increases with ageing and chronic smoking history, but prospective studies will be needed to elucidate the significance of KL-6 in chronic airway diseases.

A service review of dietetic input for chronic obstructive pulmonary disease patients on long-term oral nutritional support

Background: Patients with chronic obstructive pulmonary disease (COPD) often require long-term oral nutritional support and concomitant dietetic input, secondary to commonly associated weight loss and malnutrition (Batres, 2007). There are approximately 100 000 people in Scotland living with COPD(NHS QIS, 2009). Due to current demands on dietetic services, this retrospective case review looked to explore the number of dietetic reviews provided and the consequent change in nutritional status in a group of COPD patients. Methods: A retrospective case review of the 26 COPD patients known to the community dietetic department at the time of the study was carried out (12 females, 14 males). The patient's ranged in age from 44 to 73 with the mean (SD) age of 64 (7.5) years. Their reported heights were recorded and each patient had their weight measured on Tanita scales at each contact. Initial BMI and current BMI were then calculated, together with the number of dietetic reviews that had been provided. The results were then analysed using SPSS statistics software. Recorded BMI data was parametric therefore a paired sample T-Test was used. Results: The median number of dietetic reviews was 6 (IQR 3, 10). From this, two patient groups were formed, those receiving six or less dietetic reviews and those with over 6. The T-Test indicated a significant increase between the initial BMI and current BMI for the group receiving six or less reviews (P = <0.005). This was not significant for the group who received over six reviews. Table 1. Mean (SD) body mass index (BMI) according to number of dietetic reviews BMI on referral (kg m-2) Current BMI (kg m-2) P value Six or less dietetic reviews (n = 14) 18.1 ± 3.3 19.6 ± 3.4 ≤0.005 Over six dietetic reviews (n = 12) 18.5 ± 1.9 18.2 ± 2.3 0.424 Discussion: This review supports previous research that dietary counseling and food fortification has a positive impact on the nutritional status of COPD patients (Weekes, 2009). It indicates that dietetic input is valuable, however, due to current demands on dietetic services, it is not beneficial to continually review this patient group long-term, once nutritional stability has been established, e.g. <5% weight loss in 3–6 months (BAPEN, 2004). Due to the clinical nature of the study, the limitations included the variable timescales for dietetic reviews. Conclusion: Dietetic input has a positive effect on BMI status in COPD patients however more efficient dietetic practices need to be implemented for long-term oral nutritional support patients.

Autonomic dysfunction in patients with chronic obstructive pulmonary disease (COPD).

It has been recognized that chronic obstructive pulmonary disease (COPD) is a systemic disease which has been shown to negatively affect the cardiovascular and autonomic nerve system. The complexity of the physiologic basis by which autonomic dysfunction occurs in patients with COPD is considerable and the knowledge in this field remains elementary. The purpose of this review is to provide an overview of important potential mechanisms which might affect the autonomic nervous system in patients with COPD. This review aims to summarize the basic research in the field of autonomic dysfunction in patients with COPD. In COPD patients the activity of sympathetic nerves may be affected by recurrent hypoxemia, hypercapnia, increased intrathoracic pressure swings due to airway obstruction, increased respiratory effort, systemic inflammation and the use of betasympathomimetics. Furthermore, experimental findings suggest that autonomic dysfunction characterized by a predominance of sympathetic activity can significantly modulate further inflammatory reactions. The exact relationship between autonomic dysfunction and health status in COPD remains to be elucidated. Treatment aimed to restore the sympathovagal balance towards a reduction of resting sympathetic activity may modulate the inflammatory state, and possibly contributes to improved health status in COPD.

Pulmonary Function Testing After Stereotactic Body Radiotherapy to the Lung

Surgical resection remains the standard of care for operable early-stage non-small-cell lung cancer (NSCLC). However, some patients are not fit for surgery because of comorbidites such as chronic obstructive pulmonary disease (COPD) and other medical conditions. We aimed to evaluate pulmonary function and tumor volume before and after stereotactic body radiotherapy (SBRT) for patients with and without COPD in early-stage lung cancer. A review of prospectively collected data of Stage I and II lung cancers, all treated with SBRT, was performed. The total SBRT treatment was 60 Gy administered in three 20 Gy fractions. The patients were analyzed based on their COPD status, using their pretreatment pulmonary function test cutoffs as established by the American Thoracic Society guidelines (forced expiratory volume [FEV]% ≤ 50% predicted, FEV%/forced vital capacity [FVC]% ≤ 70%). Changes in tumor volume were also assessed by computed tomography. Of a total of 30 patients with Stage I and II lung cancer, there were 7 patients in the COPD group (4 men, 3 women), and 23 in t he No-COPD group (9 men, 14 women). At a mean follow-up time of 4 months, for the COPD and No-COPD patients, pretreatment and posttreatment FEV% was similar: 39 ± 5 vs. 40 ± 9 (p = 0.4) and 77 ± 0.5 vs. 73 ± 24 (p = 0.9), respectively. The diffusing capacity of the lungs for carbon monoxide (DL(CO)) did significantly increase for the No-COPD group after SBRT treatment: 60 ± 24 vs. 69 ± 22 (p = 0.022); however, DL(CO) was unchanged for the COPD group: 49 ± 13 vs. 50 ± 14 (p = 0.8). Although pretreatment tumor volume was comparable for both groups, tumor volume significantly shrank in the No-COPD group from 19 ± 24 to 9 ± 16 (p < 0.001), and there was a trend in the COPD patients from 12 ± 9 to 6 ± 5 (p = 0.06). SBRT did not seem to have an effect on FEV(1) and FVC, but it shrank tumor volume and improved DL(CO) for patients without COPD.

Impaired health status and care dependency in patients with advanced COPD or chronic heart failure.

PurposeAims of this cross-sectional study were to assess health status and care dependency in patients with advanced chronic obstructive pulmonary disease (COPD) or chronic heart failure (CHF) and to identify correlates of an impaired health status.MethodsThe following outcomes were assessed in outpatients with advanced COPD (n = 105) or CHF (n = 80): clinical characteristics; general health status (EuroQol-5 Dimensions (EQ-5D); Assessment of Quality of Life instrument (AQoL); Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36)); disease-specific health status (St. Georges Respiratory Questionnaire (SGRQ), Minnesota Living with Heart Failure Questionnaire (MLHFQ)); physical mobility (timed ‘Up and Go’ test); and care dependency (Care Dependency Scale).ResultsPatients with advanced COPD or CHF have an impaired health status and may be confronted with care dependency. Multiple regression analyses have shown that physical and psychological symptoms, care dependency and number of drugs were correlated with impaired health status in advanced COPD or CHF, while demographic and clinical characteristics like age, gender, disease severity and co-morbidities were not correlated.ConclusionsClinical care should regularly assess symptom burden and care dependency to identify patients with advanced COPD or CHF at risk for an impaired health status.

Lung Volumes and Emphysema in Smokers with Interstitial Lung Abnormalities

Cigarette smoking is associated with emphysema and radiographic interstitial lung abnormalities. The degree to which interstitial lung abnormalities are associated with reduced total lung capacity and the extent of emphysema is not known. We looked for interstitial lung abnormalities in 2416 (96%) of 2508 high-resolution computed tomographic (HRCT) scans of the lung obtained from a cohort of smokers. We used linear and logistic regression to evaluate the associations between interstitial lung abnormalities and HRCT measurements of total lung capacity and emphysema. Interstitial lung abnormalities were present in 194 (8%) of the 2416 HRCT scans evaluated. In statistical models adjusting for relevant covariates, interstitial lung abnormalities were associated with reduced total lung capacity (-0.444 liters; 95% confidence interval [CI], -0.596 to -0.292; P<0.001) and a lower percentage of emphysema defined by lung-attenuation thresholds of -950 Hounsfield units (-3%; 95% CI, -4 to -2; P<0.001) and -910 Hounsfield units (-10%; 95% CI, -12 to -8; P<0.001). As compared with participants without interstitial lung abnormalities, those with abnormalities were more likely to have a restrictive lung deficit (total lung capacity <80% of the predicted value; odds ratio, 2.3; 95% CI, 1.4 to 3.7; P<0.001) and were less likely to meet the diagnostic criteria for chronic obstructive pulmonary disease (COPD) (odds ratio, 0.53; 95% CI, 0.37 to 0.76; P<0.001). The effect of interstitial lung abnormalities on total lung capacity and emphysema was dependent on COPD status (P<0.02 for the interactions). Interstitial lung abnormalities were positively associated with both greater exposure to tobacco smoke and current smoking. In smokers, interstitial lung abnormalities--which were present on about 1 of every 12 HRCT scans--were associated with reduced total lung capacity and a lesser amount of emphysema. (Funded by the National Institutes of Health and the Parker B. Francis Foundation; ClinicalTrials.gov number, NCT00608764.).