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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EThe newest findings in chronic obstructive pulmonary disease (COPD) were discussed by a panel that addressed recent clinical trials, an update of COPD exacerbations, recent developments in COPD comorbidities, and a report on the COPDGene study.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EChronic Obstructive Pulmonary Disease\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPulmonary Genomics\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EChronic Obstructive Pulmonary Disease\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPulmonary Genomics\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EPulmonary \u0026amp; Respiratory Medicine\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EThe newest findings in chronic obstructive pulmonary disease (COPD) were discussed by a panel that addressed recent clinical trials, an update of COPD exacerbations, recent developments in COPD comorbidities, and a report on the COPDGene study.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EBarry J. Make, MD, National Jewish Health, Denver, Colorado, USA, delivered an update on clinical trials in COPD. In a study of 1142 patients, 250-mg once-daily azithromycin, added to usual treatment, reduced the risk of COPD exacerbations by 27% when compared with usual care [Albert RK et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2011]. The time to a first exacerbation was longer in the azithromycin group, and quality of life was improved. Inclusion criteria in this trial made it unlike other clinical trials in COPD\u2014namely, a history of oxygen use and patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage IV disease (very severe). Forty-eight percent of the participants were on triple therapy at entry. In a more recent study, patients with GOLD stage IV disease, smokers, and patients aged \u2264 65 years were less likely to respond to azithromycin [Han MK et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2014]. On the basis of these results, to reduce the risk of acute exacerbations in patients with COPD, Dr Make suggested considering azithromycin (off-label) for patients with GOLD stage II and III disease, nonsmokers, and older patients.\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EStep-down withdrawal of inhaled corticosteroids (ICSs) in patients with COPD with a history of exacerbation was not associated with an increase in the rate of moderate or severe COPD exacerbations compared with continuation of ICSs [Magnussen H et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014]. The data suggest that starting an ICS on top of dual bronchodilators is not necessary if the goal is reduction of exacerbations, said Dr Make.\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EDual bronchodilation improved trough forced expiratory volume at 1 second (FEV\u003Csub\u003E1\u003C\/sub\u003E) when compared with placebo and single-agent bronchodilation over 26 weeks (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Bateman ED et al. \u003Cem\u003EEur Respir J.\u003C\/em\u003E 2013] and improved shortness of breath as compared with placebo and single-agent bronchodilation over 6 weeks [Mahler DA et al. \u003Cem\u003EEur Respir J.\u003C\/em\u003E 2014].\u003C\/p\u003E\u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/45\/30\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Effect of Dual- vs Single-Agent Bronchodilation and Placebo on FEV1\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-1593292074\u0022 data-figure-caption=\u0022Effect of Dual- vs Single-Agent Bronchodilation and Placebo on FEV1\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/45\/30\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/45\/30\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/45\/30\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/15517\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n            \u003Cp id=\u0022p-6\u0022 class=\u0022first-child\u0022\u003EEffect of Dual- vs Single-Agent Bronchodilation and Placebo on FEV1\u003C\/p\u003E\n         \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003EFEV\u003Csub\u003E1\u003C\/sub\u003E, forced expiratory volume at 1 second.\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-2\u0022\u003E*\u003Cem\u003EP\u003C\/em\u003E \u0026lt; .001.\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-3\u0022\u003EAdapted from Bateman ED et al. Dual bronchodilation with QVA149 vs single bronchodilator therapy: the SHINE study. \u003Cem\u003EEur Respir J.\u003C\/em\u003E 2013;42:1484\u20131494.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-7\u0022\u003ESo-called comprehensive care management\u2014consisting of education, an action plan, and proactive telephone case management\u2014failed to decrease the rate of hospitalizations in patients with COPD and was associated with an increase in mortality compared with usual care [Fan VS et al. \u003Cem\u003EAnn Intern Med.\u003C\/em\u003E 2012]. Dr Make questioned whether the intervention was actually comprehensive enough to be expected to have a positive impact.\u003C\/p\u003E\u003Cp id=\u0022p-8\u0022\u003EHigh-dose N-acetylcysteine, 600 mg twice daily, reduced the frequency of COPD exacerbations as compared with placebo over 1-year follow-up, with no change in dyspnea, quality of life, or 6-minute walk distance [Tse HN et al. \u003Cem\u003EChest\u003C\/em\u003E. 2013].\u003C\/p\u003E\u003Cp id=\u0022p-9\u0022\u003ESanjay Sethi, MD, University at Buffalo, Buffalo, New York, USA, provided an update on studies of COPD exacerbations that may change practice relating to steroid use, antibiotics, and unreported exacerbations.\u003C\/p\u003E\u003Cp id=\u0022p-10\u0022\u003EThe REDUCE trial [Leuppi JD et al. \u003Cem\u003EJAMA\u003C\/em\u003E. 2013] demonstrated that in patients with acute exacerbations of COPD, 5 days of systemic corticosteroid therapy was associated with comparable outcomes and a 1-day shorter length of stay when compared with 14 days of therapy, achieving a 65% reduction in steroid dose. The study suggests that a rethinking of high-dose prolonged steroid use to treat exacerbations is in order, said Dr Sethi.\u003C\/p\u003E\u003Cp id=\u0022p-11\u0022\u003ETwo studies showed that treating bacterial COPD exacerbations with corticosteroids may do harm, possibly by having an unfavorable effect on the microbiome. In outpatients with complicated bacterial acute exacerbation of COPD, clinical failure rates were higher with oral corticosteroid use in patients treated with antimicrobials [Wilson R et al. \u003Cem\u003EEur Respir J.\u003C\/em\u003E 2012]. Patients with neutrophilic bacterial-dominant exacerbations had higher rates of treatment failure with corticosteroid treatment when compared with placebo in a biomarker-directed randomized study [Bafadhel M et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2012].\u003C\/p\u003E\u003Cp id=\u0022p-12\u0022\u003EStudies support the concept of antimicrobial treatment of acute exacerbations. Outpatients with mild to moderate acute exacerbations had a 73-day delay in their next exacerbation when treated with amoxicillin\/clavulanate versus placebo [Llor C et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2012]. Clinical failure rates with moxifloxacin were noninferior to amoxicillin\/clavulanate in a randomized controlled trial of patients with acute outpatient COPD exacerbations [Wilson R et al. \u003Cem\u003EEur Respir J.\u003C\/em\u003E 2012]. In this study, bacteriologic response at the end of therapy correlated with clinical cure at week 8 posttherapy.\u003C\/p\u003E\u003Cp id=\u0022p-13\u0022\u003EIn patients hospitalized with an acute exacerbation, 200 mg of doxycycline added to systemic corticosteroids for 7 days was no better than placebo on the outcomes of clinical cure or success at 30 days [Daniels JM et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2010]. The lesson from this study, said Dr Sethi, is that inadequate antibiotic therapy of an exacerbation can lead to frequent failures and relapses.\u003C\/p\u003E\u003Cp id=\u0022p-14\u0022\u003EPatients with moderate to very severe COPD (GOLD stage II to IV) with \u2265 2 exacerbations (or \u2265 1 resulting in hospitalization) who are on optimal conventional management and are compliant with their treatment are candidates for macrolide treatment to reduce the frequency of exacerbations, while patients with unstable cardiovascular disease or hearing loss would not be candidates [Parameswaran GI, Sethi S. \u003Cem\u003ECMAJ\u003C\/em\u003E. 2014].\u003C\/p\u003E\u003Cp id=\u0022p-15\u0022\u003EA significant proportion of COPD exacerbations are unreported. An assessment of the performance of the Exacerbations of Chronic Pulmonary Disease Tool (EXACT)\u2014a 14-question patient-reported outcome measure of COPD exacerbations\u2014in 3 randomized controlled clinical trials found that 70% to 90% of EXACT-defined events were unreported [Leidy NK et al. \u003Cem\u003EAnn Am Thorac Soc.\u003C\/em\u003E 2014]. In addition, only half of medically treated moderate events and 42% to 85% of medically treated severe events met the EXACT-defined threshold of an event, which raises uncertainty about how clinical events are defined, said Dr Sethi. Many of the unreported exacerbations are likely bacterial events, as bacterial colonization of the lower respiratory tract has been shown to increase daily symptoms in patients with COPD [Desai H et al. \u003Cem\u003EAnn Am Thorac Soc.\u003C\/em\u003E 2014].\u003C\/p\u003E\u003Cp id=\u0022p-16\u0022\u003ENicola A. Hanania, MD, Baylor College of Medicine, Houston, Texas, USA, discussed recent developments in the comorbidities of COPD. More than half of patients with COPD report \u2265 4 comorbidities [Vanfleteren LE et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2013]. In the ECLIPSE study [Miller J et al. \u003Cem\u003ERespir Med.\u003C\/em\u003E 2013], the most common COPD comorbidities reported were reflux, depression requiring treatment, and anxiety or panic attacks. Anxiety and depression in COPD patients led to an increase in symptoms, worse quality of life, and poorer functional status.\u003C\/p\u003E\u003Cp id=\u0022p-17\u0022\u003ESystemic inflammation appears to be an important pathway that links COPD with its comorbidities, said Dr Hanania. Comorbidities are related to poor outcomes and increased mortality. A greater number of comorbidities in people with impaired lung function was associated with a shorter time to first hospitalization over 5-year follow-up [Mannino DM et al. \u003Cem\u003EEur Respir J.\u003C\/em\u003E 2008]. The number of comorbidities in COPD also correlates with mortality: 3 comorbidities double the risk of mortality, and \u2265 4 are associated with a \u0026gt;4-fold risk of mortality when compared with no comorbidities [Miller J et al. \u003Cem\u003ERespir Med.\u003C\/em\u003E 2013]. Comorbidities also increase the cost of care in patients with COPD [Simon-Tuval T et al. \u003Cem\u003ERespir Res.\u003C\/em\u003E 2011]. Anemia, which can occur in 15% of patients with COPD, correlates with systemic inflammation and is associated with more hospitalizations and duration of hospitalization [Chambellan A et al. \u003Cem\u003EChest\u003C\/em\u003E. 2005].\u003C\/p\u003E\u003Cp id=\u0022p-18\u0022\u003EThe prevalence of osteoporosis increases with COPD disease severity. When emphysema is present, the odds of osteopenia\/osteoporosis increase \u0026gt;2-fold [Bon J et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2011]. Weight loss and muscle wasting are common in COPD. Increased breakdown of muscle proteins, a feature typical of cachexia, has been demonstrated in underweight patients with COPD [Agust\u00ed AG et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2002].\u003C\/p\u003E\u003Cp id=\u0022p-19\u0022\u003EThe effects of current treatments for COPD, except for pulmonary rehabilitation, on comorbidities have not been researched in prospective studies. The treatment of comorbidities in patients with COPD should be similar to treatment in patients without COPD, Dr Hanania said. Future studies of novel interventions for COPD should include patients with comorbidities.\u003C\/p\u003E\u003Cp id=\u0022p-20\u0022\u003EDr Make closed the session by offering lessons learned from some of the many analyses of the COPDGene study population. The goals of the study are to define genetic associations with COPD, phenotypes of COPD, pathophysiologic and mechanistic factors, the factors influencing disease progression, and the factors influencing response to therapy. It includes 10 059 patients with COPD (smokers, ex-smokers, and nonsmokers).\u003C\/p\u003E\u003Cp id=\u0022p-21\u0022\u003EOf the first 2500 patients, 1061 have GOLD stages II to IV (290 with chronic bronchitis and 771 without). A study of the chronic bronchitic phenotype found that chronic bronchitis in COPD is associated with worse respiratory symptoms and almost twice the risk of exacerbations [Kim V et al. \u003Cem\u003EChest\u003C\/em\u003E. 2011]. Predictors of chronic bronchitis in COPD are histories of asthma, allergic rhinitis, and acute bronchitis; current smoking; a lower FEV\u003Csub\u003E1\u003C\/sub\u003E; Caucasian race; male sex; and airway thickening [Kim V et al. \u003Cem\u003ERespir Res.\u003C\/em\u003E 2014]. Relative to controls without chronic bronchitis, genome-wide significant associations with chronic bronchitis were found on 4q22.1 (\u003Cem\u003EFAM13A\u003C\/em\u003E) and 11p15.5 (\u003Cem\u003EEFCAB4A\u003C\/em\u003E, \u003Cem\u003ECHID1\u003C\/em\u003E, and \u003Cem\u003EAP2A2\u003C\/em\u003E) and a locus associated with chronic bronchitis on 1q23.3 (\u003Cem\u003ERPL31P11\u003C\/em\u003E and \u003Cem\u003EATF6\u003C\/em\u003E) [Lee JH et al. \u003Cem\u003ERespir Res.\u003C\/em\u003E 2014].\u003C\/p\u003E\u003Cp id=\u0022p-22\u0022\u003EQuantitative computed tomography (CT) reveals that acute exacerbations of COPD are more frequent with worse emphysema and airway disease. Quantitative CT-defined airway disease was found to be more closely associated with worse quality of life on the St George\u0027s Respiratory Questionnaire than emphysema was [Martinez CH et al. \u003Cem\u003EThorax\u003C\/em\u003E. 2012]. The same study found that emphysema is more closely associated with the BODE index than airway disease is. Other lessons learned from chest CT scans are that interstitial lung abnormalities are common in smokers with COPD and that interstitial lung abnormalities is associated with a greater burden of disease [Doyle TJ et al. \u003Cem\u003EAm J Respir Crit Care Med.\u003C\/em\u003E 2012].\u003C\/p\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2014 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/14\/45\/30.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzoik2\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzoik2\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}