Patient–Physician Communication About End-of-Life Care for Patients with Severe COPD; J. R. Curtis, R. A. Engelberg, E. L. Nielsen, D. H. Au, D. L. Patrick (Eur Respir J 2004; 24:200–205).
Since patients with chronic obstructive pulmonary disease (COPD) infrequently discuss treatment preferences about end-of-life care with physicians, the goal of the present study was to identify which specific areas of communication about end-of-life care occur between patients with severe COPD and their physicians, and how patients rate the quality of this communication.
A total of 115 patients with oxygen-dependent COPD, identified in pulmonary clinics in three hospitals and through an oxygen delivery company, were enrolled in this study. A 17-item quality of communication questionnaire (QOC) was administered to patients, along with other measures, including satisfaction with care.
The patients reported that most physicians do not discuss how long the patients have to live, what dying might be like, or patients' spirituality. Patients rated physicians highly at listening and answering questions. Areas patients rated relatively low included discussing prognosis, what dying might be like, and spirituality/religion. Patients' assessments of physicians' overall communication and communication about treatment correlated well with the QOC. Patients' overall satisfaction with care also correlated significantly with the QOC.
In conclusion, this study identifies areas of communication that physicians do not address and areas that patients rate poorly, including talking about prognosis, dying, and spirituality. These areas may provide targets for interventions to improve communication about end-of-life care for patients with chronic obstructive pulmonary disease. Future studies should determine the responsiveness of these items to interventions, and the effect such interventions have on patient satisfaction and quality of care.
Comments. The authors point out that the Gold Guidelines suggest that discussions regarding end of life care should be had with patients with severe COPD but actual recommendations about this issue are lacking. The study finds that there are still significant areas that physicians fail to address with patients regarding survival and what it may be like to die. The Quality of Communication Questionnaire was initially developed to study AIDS patients but it was extensively modified to address issues important for COPD patients (reference provided for online access). The authors point out the study is limited by the fact that only 50% responded to the questionnaire (likely representing a biased group) and that it took place in only one city. The QOC questionnaire will need to be evaluated further for its validity and reliability. Even more important, however, is that further studies are clearly required to identify patients' needs in this regard and the best ways to prepare physicians to address these issues with patients and to assess the impact in terms of quality of life and indeed quality of death for patients with severe COPD.
Characteristics of Airway Inflammation and Bronchodilator Reversibility in COPD A Potential Guide to Treatment; D.-W. Perng, H.-Y. Huang, H.-M. Chen, Y.-C. Lee, R.-P. Perng (Chest 2004; 126:375–381).
Study Objectives. The management of stable patients with COPD depends on the severity of symptoms and airflow limitation. Regarding inflammation, corticosteroids are the only medications that are recommended for use, and only under restricted circumstances. Corticosteroids tend to undertreat or overtreat patients with COPD when only clinical manifestations and the findings of simple spirometry are considered. Accordingly, our aim was to survey the characteristics of airway inflammation in stable COPD patients, and to assess the interrelations among inflammatory cells, inflammatory mediators, bronchodilator reversibility, and pulmonary function. Factors related to airway inflammation and bronchodilator reversibility may be important in the management of stable COPD patients.
Methods. A total of 88 stable patients with smoking-related COPD were recruited into the study. All patients were steroid-free, and had been treated with theophylline, oral ß2-agonist agents, anticholinergic agents, and possibly mucolytic agents. Bronchodilator tests and sputum induction were performed to evaluate bronchodilator reversibility, and numbers of inflammatory cells and mediators (eg., interleukin [IL]-8, eotaxin, and regulated on activation, normal T cells expressed and secreted [RANTES]).
Results. Thirty-one of 48 patients (64.6%) who had bronchodilator reversibility, and 19 of 40 patients (47.5%) without bronchodilator reversibility had sputum eosinophilia (median, 8.0% and 7.0%, respectively). FEV1 showed a significant inverse correlation with the number of sputum neutrophils. The correlation coefficient for post-bronchodilator FEV1 vs the percentage of neutrophils in patients with non-reversible COPD was higher than that in those with reversible COPD. The levels of IL-8 were closely associated with the percentage of neutrophils. The sputum concentrations of IL-8 and albumin were significantly higher in patients with nonreversible COPD than in those with reversible COPD. A significant inverse correlation was found between bronchodilator response (i.e., ΔFEV1 and ΔFVC) and prebronchodilator FEV1.
Conclusions. Eosinophilic inflammation may play a substantial role in COPD, while neutrophils and IL-8 may have a great influence on non-reversible obstructive airways. The assessment of airway inflammation and bronchodilator responses can help the selection of specific therapies and the prediction of clinical outcomes for COPD patients.
Key Words: COPD, Eosinophils, Induced sputum, Neutrophils, Reversibility.
Comments. Understanding the relationship between patterns of inflammation and physiological consequences may be important for making rationale decisions with regard to current and future (likely expensive) anti-inflammatory therapeutic agents. This study finds sputum eosinophilia is not uncommon in COPD patients and is not predictive of bronchodilator response (BDR). The lack of elevated levels of eotaxin or RANTES in the COPD patients with sputum eosinophilia compared to controls argues that these are not asthmatics contaminating the sample. Sputum levels of albumin, IL-8, and neutrophils were higher in patients with no BDR. Whether they play an active role in reducing BDR or are merely associated with it requires further study. This study did not examine whether these biomarkers predict steroid responsiveness. It is clear that the characterization of COPD as not involving eosinophils (or mast cells for that matter) is an oversimplification of the complexity and heterogeneity of airway inflammation in COPD and that the roles of various inflammatory mediators in the pathogenesis of COPD remains an important area for further study.
Relationship Between Peripheral Airway Dysfunction, Airway Obstruction, and Neutrophilic Inflammation in COPD; R. A. O'Donnell, C. Peebles, J. A. Ward, A. Daraker, G. Angco, P. Broberg, S. Pierrou, J. Lund, S. T. Holgate, D. E. Davies, D. J. Delany, S. J., Wilson, R. Djukanovic (Thorax 2004; 59:837–842).
Background. Considerable research has been conducted into the nature of airway inflammation in chronic obstructive pulmonary disease (COPD), but the relationship between proximal airways inflammation and both dynamic collapse of the peripheral airways and HRCT-determined emphysema severity remains unknown. A number of research tools have been combined to study smokers with a range of COPD severities classified according to the GOLD criteria.
Methods. Sixty-five subjects (11 healthy smokers, 44 smokers with stage 0–IV COPD, and 10 healthy non-smokers) were assessed using lung function testing and HRCT scanning to quantify emphysema and peripheral airway dysfunction and sputum induction to measure airway inflammation.
Results. Expiratory HRCT measurements and the expiratory/inspiratory mean lung density ratio (both indicators of peripheral airway dysfunction) correlated more closely in smokers with the severity of airflow obstruction (r = − 0.64, p < 0.001) than did inspiratory HRCT measurements (which reflect emphysema severity; r = − 0.45, p < 0.01). Raised sputum neutrophil counts also correlated strongly in smokers with HRCT indicators of peripheral airway dysfunction (r = 0.55, p < 0.001) but did not correlate with HRCT indicators of the severity of emphysema.
Conclusions. This study suggests that peripheral airway dysfunction, assessed by expiratory HRCT measurements, is a determinant of COPD severity. Airway neutrophilia, a central feature of COPD, is closely associated with the severity of peripheral airway dysfunction in COPD but is not related to the overall severity of emphysema as measured by HRCT.
Comments. In this article the authors found that sputum neutrophilia was correlated to the severity of peripheral airway dysfunction as documented by HRCT measures of mean lung density (MLD) during expiration versus inspiration (E/I) ratio. Sputum neutrophilia was not correlated to severity of emphysema quantified by using % area of low attenuation (LAA) or MLD values seperately (as opposed to the E/I ratio). Interestingly the mean lung density E/I ratio was highest in the GOLD COPD classifications II-IV largely as a result of the expiratory MLD being lower (i.e., more negative) in this group rather than the inspiratory MLD being higher (i.e., less negative). Subjects were screened for recent or current infections by history and culture, respectively, and presumably elevated % neutrophil counts in these subjects did not indicate cases of active infection although subclinical bacterial colonization was not ruled out. This study also found that lung function correlated moderately strongly with HRCT parameters, particularly the E/I ratio compared to FEV1%, MEF50, and RV/TLC and that these lung function parameters also correlated with sputum neutrophilia. HRCT as a noninvasive method of evaluating COPD appears to provide best assessment of emphysema using inspiratory %LAA and best assessment of functional impairment using MLD E/I ratios during expiration. The actual role of neutrophils in the pathogenesis of peripheral airway dysfunction remains an area requiring further study.
Effects of Fluticasone on Systemic Markers of Inflammation in Chronic Obstructive Pulmonary Disease; D. D. Sin, P. Lacy, E. York, S. F. P. Man (Am J Respir Crit Care Med 2004; 170:760–765).
Systemic inflammation is present in chronic obstructive pulmonary disease (COPD), which has been linked tocardiovascular morbidity and mortality. We determined the effects of oral and inhaled corticosteroids on serum markers of inflammation in patients with stable COPD. We recruited 41 patients with mild-to-moderate COPD. After 4 weeks during which inhaled corticosteroids were discontinued, patients were assigned to fluticasone (500 mcg twice a day), oral prednisone (30 mg/day), or placebo over 2 weeks, followed by 8 weeks of fluticasone at 500 mcg twice a day and another 8 weeks at 1,000 mcg twice a day. Withdrawal of inhaled corticosteroids increased baseline C-reactive protein (CRP) levels by 71% (95% confidence interval [CI], 16–152%). Two weeks with inhaled fluticasone reduced CRP levels by 50% (95% CI, 9–73%); prednisone reduced it by 63% (95% CI, 29–81%). No significant changes were observed with the placebo. An additional 8 weeks of fluticasone were associated with CRP levels that were lower than those at baseline (a 29% reduction; 95% CI, 7–46%). Inhaled and oral corticosteroids are effective in reducing serum CRP levels in patients with COPD and suggest their potential use for improving cardiovascular outcomes in COPD.
Key Words: Chronic obstructive pulmonary disease, Corticosteroid, C-reactive protein, Fluticasone, Prednisone.
Comments. Cardiovascular disease remains the greatest cause for mortality in the United States followed by COPD. Great interest has developed considering the role of systemic inflammation and its contribution to risk of cardiovascular disease. COPD is recognized to have a systemic inflammatory component and hence may contribute to the increased risk of coronary artery disease seen in COPD patients. The study by Sin and colleagues suggests that inhaled corticosteroids are able to reduce markers of systemic inflammation such as CRP almost as much as 30 mg of Prednisone. It remains unanswered whether inhaled corticosteroids exert such effects directly through absorption into the systemic circulation or via second messengers released from the airways that then enter the circulation and inhibit CRP production. Regardless, the potential for ICS to exert some effect on systemic inflammatory markers that are associated with increased cardiovascular risk and whether such treatment may reduce cardiovascular related morbidity and mortality will undoubtedly be an area of intense investigation in the future.