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Takefumi Saito,1 Akinori Takeda,2 Katsuji Hashimoto,3 Akihiro Kobayashi,4 Tomoyuki Hayamizu,5 Gerald W Hagan6 1Department of Respiratory Medicine, Ibarakihigashi National Hospital, Naka, Ibaraki, 2Center for Pulmonary Medicine, Asahikawa Medical Center, Asahikawa, Hokkaido, 3AMC Nishiumeda Clinic, Osaka, 4Biomedical Science Department, 5Medical Affairs Respiratory Department, GlaxoSmithKline KK, Tokyo, Japan; 6Independent Consultant, Marbella, Spain Purpose: Triple therapy using salmeterol/fluticasone propionate (FP) and tiotropium bromide is commonly used to treat chronic obstructive pulmonary disease (COPD), but sparse efficacy data exist in COPD patients with fewer symptoms and with a lower dose of inhaled corticosteroid in Japanese patients. The effects of of salmeterol/fluticasone propionate 50/250 µg (SFC250) twice daily plus tiotropium 18 µg (TIO) once daily and individual treatments on lung function were compared. Patients and methods: Fifty three Japanese COPD patients participated in this randomized, double-blind, double-dummy, Williams square design crossover study. Lung function was assessed by plethysmography and spirometry. Results: The primary endpoint of postdose specific airway conductance area under the curve (AUC0–4h) on day 28 was significantly higher following SFC250 + TIO (0.854) compared with TIO (0.737, 15.8%) and SFC250 (0.663, 28.8%) alone. SFC250 + TIO significantly improved trough forced expiratory volume in 1 second from baseline versus TIO (0.161 L, P

Saito T, Takeda A, Hashimoto K, et al. Int J Chron Obstruct Pulmon Dis. 2015;10:2393–2404.On page 2395, right column, line 3, “Philadelphia, PA, USA” should have read “Hoechberg, Germany”.On page 2396, Figure 2 was incorrect. The corrected figure is shown.On page 2396, right column, line 1, “although FEV1 and FVC were not log transformed prior to analysis” should have read “although sRaw and sGaw were log transformed prior to analysis”.On page 2397, right column, Lung volumes section, line 5, “Statistical significance was observed for postdose RV immediately after dosing (time =0) on day 28 for SFC250 + TIO compared to TIO and SFC250 (Tables S3, S4). Improvements on day 28 were also seen in postdose TGV, IC, and TLC following treatment with SFC250 + TIO compared to each component, but none were significant (Table S4). Improvements were seen for all parameters for their adjusted mean values on day 1, but none were significant (Table S3).” Should have read “Statistical significance was observed for trough RV (time =0) on day 28 for SFC250 + TIO compared to TIO and SFC250 (Table S3). Improvements on day 28 were also seen in postdose TGV, IC, and TLC following treatment with SFC250 + TIO compared to each component, but statistical treatment differences were not observed, except for after dosing (240 min) IC at day 28 (Table S3). Improvements were seen for all parameters for their adjusted mean values on day 1, but statistical treatment differences were not observed, except for SFC250 after dosing (240 min) TGV at day 1 (Table S3).”On page 2398, Figure 3 was incorrect. The corrected figure is shown.On page 2398, Table 3, TGV (L) row, SFC250 + TIO vs TIO (n=50): 97.5% CI column, “-0.029” should have read “0.029”.On page 2398, Table 3, TGV (L) row, SFC250 + TIO vs SFC250 (n=50): 97.5% CI column, “-0.028” should have read “0.028”.On page 2398, Table 3, Note section, “Difference” should have read “Adjusted mean difference”.On page 2402, Table S2, figure caption, “Postdose raw mean (standard deviation log) values of sGaw and sRaw (mITT population)” should have read “Postdose raw geometric mean (standard deviation log) values of sGaw and sRaw (mITT population)”.On page 2402, Table S2, Time (minutes) column, sGaw, third line down, “SFC250 + TIO” should have read “SFC250”.On page 2402, Table S2, Time (minutes) column, sRaw, third line down, “SFC250 + TIO” should have read “SFC250”.Read the original article

Katsuya Onishi,1 Daisuke Yoshimoto,2 Gerry W Hagan,3 Paul W Jones4 1Onishi Heart Clinic, Mie, 2Medical Affairs Respiratory, GlaxoSmithKline KK, Tokyo, Japan; 3Independent Consultant, Marbella, Spain; 4Division of Clinical Science, St George's, University of London, London, UK Background and objectives: Cardiovascular disease (CVD) and chronic obstructive pulmonary disease (COPD) commonly coexist and share common risk factors. The prevalence of COPD in outpatients with a smoking history and CVD in Japan is unknown. The aim of this study was to determine the proportion of Japanese patients with a smoking history being treated for CVD who have concurrent airflow limitation compatible with COPD. A secondary objective was to test whether the usage of lung function tests performed in the clinic influenced the diagnosis rate of COPD in the patients identified with airflow limitation. Methods: In a multicenter observational prospective study conducted at 17 centers across Japan, the prevalence of airflow limitation compatible with COPD (defined as forced expiratory volume (FEV)1/FEV6

Impact: This study explores the use of measuring plasma biomarkers at exacerbation of chronic obstructive pulmonary disease (COPD), providing insight into the underlying pathogenesis of these important events. Rationale: The use of measuring C-reactive protein (CRP) to confirm exacerbation, or to assess exacerbation severity, in COPD is unclear. Furthermore, it is not known whether there may be more useful systemic biomarkers. Objective: To assess the use of plasma biomarkers in confirming exacerbation and predicting exacerbation severity. Methods: We assessed 36 biomarkers in 90 paired baseline and exacerbation plasma samples from 90 patients with COPD. The diagnosis of exacerbation fulfilled both health care use and symptom-based criteria. Biomarker concentrations were related to clinical indices of exacerbation severity. Interrelationships between biomarkers were examined to gain information on mechanisms of systemic inflammation at exacerbation of COPD. Measurements and Main Results: To confirm the diagnosis of exacerbation, the most selective biomarker was CRP. However, this was neither sufficiently sensitive nor specific alone (area under the receiver operating characteristic curve [AUC], 0.73; 95% confidence interval, 0.66-0.80). The combination of CRP with any one increased major exacerbation symptom recorded by the patient on that day (dyspnea, sputum volume, or sputum purulence) significantly increased the AUC to 0.88 (95% confidence interval, 0.82-0.93; p < 0.0001). There were no significant relationships between biomarker concentrations and clinical indices of exacerbation severity. Interrelationships between biomarkers suggest that the acute-phase response is related, separately, to monocytic and lymphocytic-neutrophilic pathways. Conclusions: Plasma CRP concentration, in the presence of a major exacerbation symptom, is useful in the confirmation of COPD exacerbation. Systemic biomarkers were not helpful in predicting exacerbation severity. The acute-phase response at exacerbation was most strongly related to indices of monocyte function. [ABSTRACT FROM AUTHOR]

Background: Patients with Chronic Obstructive Pulmonary Disease (COPD) are at higher risk of developing Community-Acquired Pneumonia (CAP) than patients in the general population. However, no studies have been performed in general practice assessing longitudinal incidence rates for CAP in COPD patients or risk factors for pneumonia onset., Methods: A cohort of COPD patients aged ≥ 45 years, was identified in the General Research Practice Database (GPRD) between 1996 and 2005, and annual and 10-year incidence rates of CAP evaluated. A nested case-control analysis was performed, comparing descriptors in COPD patients with and without CAP using conditional logistic regression generating odds ratios (OR) and 95% confidence intervals (CI)., Results: The COPD cohort consisted of 40,414 adults. During the observation period, 3149 patients (8%) experienced CAP, producing an incidence rate of 22.4 (95% CI 21.7-23.2) per 1000 person years. 92% of patients with pneumonia diagnosis had suffered only one episode. Multivariate modelling of pneumonia descriptors in COPD indicate that age over 65 years was significantly associated with increased risk of CAP. Other independent risk factors associated with CAP were co-morbidities including congestive heart failure (OR 1.4, 95% CI 1.2-1.6), and dementia (OR 2.6, 95%CI 1.9-3.). Prior severe COPD exacerbations requiring hospitalization (OR 2.7, 95% CI 2.3-3.2) and severe COPD requiring home oxygen or nebulised therapy (OR 1.4, 95% CI 1.1-1.6) were also significantly associated with risk of CAP., Conclusion: COPD patients presenting in general practice with specific co-morbidities, severe COPD, and age >65 years are at increased risk of CAP., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Background: Many UK hospitals have set-up specialised chest pain clinics to deal promptly and efficiently with cases of possible cardiac chest pain. It is possible that a proportion of patients attending these clinics will have a respiratory cause for their chest pain, or respiratory disease in addition to their cardiac pain. This study aimed to determine the prevalence of airflow obstruction, ischaemic heart disease and dual pathology in such patients., Methods: Spirometry was performed on patients referred to a rapid access chest pain clinic over a 12-month period (target population of 400 patients). The main outcome measure was the prevalence of airflow obstruction (defined using spirometry), ischaemic heart disease and dual pathology., Results: 405 subjects participated in the study. Abnormal spirometry was detected in 21% of patients (n=85). Airflow obstruction was the predominant lung function abnormality and was detected in 60 patients. Ischaemic heart disease was diagnosed in 21% of patients (n=85). Dual pathology was found in 4% of patients (n=17)., Conclusions: Previous studies have reported a link between impaired lung function and future cardiovascular morbidity and mortality. This study suggests that airflow obstruction is an important alternative differential diagnosis in patients referred to a rapid access chest pain clinic. The identification of abnormal spirometry may help to better risk-stratify patients for future cardiovascular events and allow interventions to be instituted.

Introduction: Lung function impairment may be a risk factor for cardiovascular disease (CVD) events., Objective: To determine the relationship between the severity of airflow obstruction based on modified Global Initiative on Obstructive Lung Disease (GOLD) criteria and the prevalence and incidence or recurrence of CVD in a cohort of US adults, aged 45-64 years, from 1987 to 2001., Methods: We analysed data from 14 681 adults using logistic regression to determine the cross sectional association between lung function impairment and prevalent CVD at baseline and Cox regression to examine the prospective association of lung function impairment at baseline with CVD over 15 years of follow-up. Models were adjusted for age, sex, race, smoking, comorbid hypertension and diabetes, cholesterol levels and fibrinogen level., Results: At baseline, the crude prevalence of CVD was higher among subjects with GOLD 2 (OR 2.9, 95% CI 2.4 to 3.6) and GOLD 3 or 4 chronic obstructive pulmonary disease (COPD) (OR 3.0, 95% CI 2.0 to 4.5), compared with normal subjects. These relative risks were greatly reduced after adjusting for covariates (OR 1.4, 95% CI 1.1 to 1.8 for GOLD 2 and OR 1.3, 95% CI 0.8 to 2.1 for GOLD 3 or 4). Similarly, the association between COPD and risk of incident or recurrent CVD was much stronger in the unadjusted models (hazard ratio (HR) 2.4, 95% CI 2.1 to 2.7 for GOLD 2 and 2.9, 95% CI 2.2 to 3.9 for GOLD 3 or 4) than in the adjusted ones (HR 1.2, 95% CI 1.03 to 1.4 for GOLD 2 and 1.5, 95% CI 1.1 to 2.0 for GOLD 3 or 4)., Conclusion: We observed a crude association between lung function impairment and prevalent and incident or recurrent CVD that was greatly reduced after adjusting for covariates, including age, sex, race, smoking, comorbid hypertension and diabetes, cholesterol levels and fibrinogen level. These data suggest that this association may be, in part, mediated through established CVD risk factors included in our adjusted models.