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1.
Thorax ; 74(10): 934-940, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31481635

RESUMO

BACKGROUND: Individual susceptibility to exacerbations in chronic obstructive pulmonary disease (COPD) is likely influenced by genetic factors; however, most such variance is unexplained. We hypothesised that ß2-adrenergic receptor genotypes, Gly16Arg (rs1042713, c.46G>A) and Gln27Glu (rs1042714, c.79C>G) influence risk of severe exacerbations in COPD. METHODS: Among 96 762 individuals in the Copenhagen General Population Study, we identified 5262 with COPD (forced expiratory volume in one second divided by forced vital capacity, FEV1/FVC, below 0.7, FEV1 less than 80% of predicted value, age above 40 years and no asthma) who had genotyping performed. Severe exacerbations were defined as acute admissions due to COPD during 5 years of follow-up (mean 3.4 years). 923 individuals with COPD diagnosed similarly in the Copenhagen City Heart Study (CCHS) were used for replication analyses. RESULTS: We recorded 461 severe exacerbations in 5262 subjects. The HRs for severe exacerbations were 1.62 (95% CI 1.30 to 2.03, p=0.00002) for 16Gly/Arg heterozygotes and 1.41 (1.04 to 1.91, p=0.03) for 16Arg homozygotes, compared with 16Gly homozygotes. HRs were 1.35 (1.03 to 1.76, p=0.03) for 27Gln/Glu heterozygotes and 1.49 (1.12 to 1.98, p=0.006) for 27Gln homozygotes, compared with 27Glu homozygotes. Similar trends were observed in the CCHS. Among 27Gln homozygotes only, HRs were 5.20 (1.81 to 14.9, p=0.002) for 16Gly/Arg heterozygotes and 4.03 (1.40 to 11.6, p=0.01) for 16Arg homozygotes, compared with 16Gly homozygotes. CONCLUSION: Common ß2-adrenergic receptor genotypes influence risk of severe exacerbations in COPD, potentially mainly by genetic influence of the 16Arg allele in rs1042713.

2.
Respir Med ; 155: 141-147, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31362177

RESUMO

BACKGROUND: Differences in previous exacerbation history may influence prognosis of chronic obstructive pulmonary disease (COPD). We hypothesized that prognosis differs between individuals with a history of only medically treated exacerbations (moderate exacerbations) and those with a history of hospitalised exacerbations (severe exacerbations). METHODS: We included 98 614 adults from the Copenhagen General Population Study and assessed risk of moderate and severe exacerbations, pneumonia hospitalisation, and respiratory and all-cause mortality from 2003 until 2013 according to exacerbation history. RESULTS: Among 6545 individuals with COPD, 6290 had no exacerbations in the preceding year, 109 had one moderate exacerbation, 108 had two or more moderate exacerbations, and 38 had one or more severe exacerbations. During 9.4 years of follow-up, we observed 926 moderate and 244 severe exacerbations, 477 pneumonias, and 707 deaths, including 69 from respiratory disease. Compared to individuals without previous exacerbations, lung function and symptom adjusted hazard ratios (HRs) for future moderate exacerbation were 4.68 (95% confidence interval:3.31-6.62) for individuals with one previous moderate exacerbation, 21 (13-33) for individuals with two or more previous moderate exacerbations, and 5.30 (3.44-8.15) for individuals with one or more previous severe exacerbations. Corresponding HRs were 1.62(0.78-3.34), 1.29(0.57-2.89), and 5.43 (2.56-12) for severe exacerbation, 1.86(1.06-3.27), 1.74(1.01-2.99), and 4.85 (2.94-8.02) for pneumonia, 0.53(0.10-2.99), 1.65(0.53-5.17), and 2.98 (1.14-7.83) for respiratory mortality, and 1.34(0.79-2.29), 1.57(1.00-2.47), and 1.49 (0.85-2.62) for all-cause mortality, respectively. CONCLUSION: Individuals with COPD and a history of hospitalised exacerbations carried the poorest prognosis compared to those with a history of only medically treated exacerbations, suggesting difference in risk profile.

4.
Eur Respir J ; 2019 Jun 27.
Artigo em Inglês | MEDLINE | ID: mdl-31248954

RESUMO

A normal spirometry is often used to preclude airway disease in individuals with unspecific respiratory symptoms. We tested the hypothesis that chronic respiratory symptoms are associated with respiratory hospitalisations and death in individuals with normal spirometry without known airway disease.We included 108 246 randomly chosen individuals aged 20-100 from a Danish population-based cohort study. Normal spirometry was defined as a pre-bronchodilator forced expiratory volume in 1 s(FEV1)/forced vital capacity(FVC)≥0.70. Chronic respiratory symptoms included dyspnoea, chronic mucus hypersecretion, wheezing, and cough. Individuals with known airway disease, i.e. chronic obstructive pulmonary disease and/or asthma, were excluded (n=10 291). We assessed risk of hospitalisations due to exacerbations of airway disease and pneumonia, and respiratory and all-cause mortality from 2003 through 2018.52 999 had normal spirometry without chronic respiratory symptoms and 30 890 had normal spirometry with chronic respiratory symptoms. During follow-up, we observed 1037 hospitalisations with exacerbation of airway disease, 5743 hospitalisations with pneumonia, and 8750 deaths, of which 463 were due to respiratory disease. Compared to individuals with normal spirometry without chronic respiratory symptoms, multivariable adjusted hazard ratios for individuals with normal spirometry with chronic respiratory symptoms were 1.62(95% confidence interval:1.20-2.18) for exacerbation hospitalisations, 1.26(1.17-1.37) for pneumonia hospitalisations, 1.59(1.22-2.06) for respiratory mortality, and 1.19(1.13-1.25) for all-cause mortality. There was a positive dose-response relationship between number of symptoms and risk of outcomes. Results were similar after 2 years follow-up, for never-smokers alone, and for each symptom separately.Chronic respiratory symptoms are associated with respiratory hospitalisations and death in individuals with normal spirometry without known airway disease.

5.
Artigo em Inglês | MEDLINE | ID: mdl-31114183

RESUMO

Background: Blood eosinophils may predict response to inhaled corticosteroids (ICS) in chronic obstructive pulmonary disease (COPD) where ICS is recommended in patients at high risk of exacerbations. The proportion of patients who may benefit the most from ICS-based therapy was quantified in a real-world population. Materials and methods: European data from the Adelphi Real World Respiratory Disease Specific Programme™ 2017 survey were collected from consecutive COPD patients by participating physicians. Overall, 1,528 patients were assessable for Global Initiative for COPD (GOLD) 2017 status and were included in the analysis. Results: More GOLD D patients had elevated eosinophil counts compared with GOLD B. The proportions of GOLD D patients with a history of ≥2 exacerbations and eosinophil counts of ≥150, ≥300, and ≥400 cells/µL were 81.2%, 39.4%, and 24.6%, respectively. In total, 10.6% of the patients had ≥300 eosinophils/µL and a history of ≥2 exacerbations. ICS-based therapy was received by 41.5% of GOLD B and 68.0% of GOLD D patients. Conclusion: There was no apparent relation between ICS use and eosinophil blood count. There are differences in the distributions of patients with frequent exacerbations and/or high blood eosinophil counts and the use of ICS in COPD. These data may provide information for the implementation of future treatment recommendations.

6.
Lancet Respir Med ; 7(8): 699-709, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31122894

RESUMO

BACKGROUND: Treatment with systemic corticosteroids in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) is associated with debilitating adverse effects. Therefore, strategies to reduce systemic corticosteroid exposure are urgently required and might be offered by a personalised biomarker-guided approach to treatment. The aim of this study was to determine whether an algorithm based on blood eosinophil counts could safely reduce systemic corticosteroid exposure in patients admitted to hospital with acute exacerbations of COPD. METHODS: We did a multicentre, randomised, controlled, open-label, non-inferiority trial at the respiratory departments of three different university-affiliated hospitals in Denmark. Eligible participants were patients included within 24h of admission to the participating sites, aged at least 40 years, with known airflow limitation (defined as a post-bronchodilator FEV1/forced vital capacity [FVC] ratio ≤0·70) and a specialist-verified diagnosis of COPD, who were designated to start on systemic corticosteroids by the respiratory medicine physician on duty. We randomly assigned patients (1:1) to either eosinophil-guided therapy or standard therapy with systemic corticosteroids. Both investigators and patients were aware of the group assignment. All patients received 80 mg of intravenous methylprednisolone on the first day. The eosinophil-guided group were from the second day given 37·5 mg of prednisolone oral tablet daily (for a maximum of up to 4 days) on days when their blood eosinophil count was at least 0·3 × 109 cells per L. On days when the eosinophil count was lower, prednisolone was not administered. If a patient was discharged during the treatment period, a treatment based on the last measured eosinophil count was prescribed for the remaining days within the 5-day period (last observation carried forward). The control group received 37·5 mg of prednisolone tablets daily from the second day for 4 days. The primary outcome was the number of days alive and out of hospital within 14 days after recruitment, assessed by intention to treat (ITT). Secondary outcomes included treatment failure at day 30 (ie, recurrence of acute exacerbation of COPD resulting in emergency room visits, admission to hospital, or need to intensify pharmacological treatment), number of deaths on day 30, and duration of treatment with systemic corticosteroids. The non-inferiority margin was 1·2 days (SD 3·8). This trial is registered at ClinicalTrials.gov, number NCT02857842, and was completed in January, 2019. FINDINGS: Between Aug 3, 2016, and Sept 30, 2018, 159 patients in the eosinophil-guided group and 159 patients in the control group were included in the ITT analyses. There was no between-group difference for days alive and out of hospital within 14 days after recruitment: mean 8·9 days (95% CI 8·3-9·6) in the eosinophil-guided group versus 9·3 days (8·7-9·9) in the control group (absolute difference -0·4, 95% CI -1·3 to 0·5; p=0·34). Treatment failure at 30 days occurred in 42 (26%) of 159 patients in the eosinophil-guided group and 41 (26%) of 159 in the control group (difference 0·6%, 95% CI -9·0 to 10·3; p=0·90). At 30 days nine patients (6%) of 159 in the eosinophil-guided group and six (4%) of 159 in the control group had died (difference 1·9%, 95% CI -2·8 to 6·5; p=0·43). Median duration of systemic corticosteroid therapy was lower in the eosinophil-guided group: 2 days (IQR 1·0 to 3·0) compared with 5 days (5·0 to 5·0) in the control group, p<0·0001. INTERPRETATION: Eosinophil-guided therapy was non-inferior compared with standard care for the number of days alive and out of hospital, and reduced the duration of systemic corticosteroid exposure, although we could not entirely exclude harm on some secondary outcome measures. Larger studies will help to determine the full safety profile of this strategy and its role in the management of COPD exacerbations. FUNDING: The Danish Regions Medical Fund and the Danish Council for Independent Research.

7.
Respir Res ; 20(1): 63, 2019 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-30935391

RESUMO

BACKGROUND: Identifying subjects with chronic obstructive pulmonary disease (COPD) at high risk of exacerbation and mortality is key to aid individual management of COPD. The only FDA approved blood-based drug development biomarker for patients at high risk of mortality, is plasma fibrinogen. In this study, we benchmarked two biomarkers of basement membrane remodeling, a characteristic of COPD, against plasma fibrinogen alone and as a combination. The biomarkers of basement membrane remodeling are two neoepitopes from of the alpha 3 chain of type IV collagen (COL4A3). MATERIALS AND METHODS: COL4A3 degradation was assessed by the biomarkers C4Ma3 and tumstatin (TUM) in year 1 plasma samples in 984 COPD subjects, 95 non-smoking controls and 95 smoking controls from the Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE) cohort. They were measured by competitive ELISA using monoclonal antibodies recognizing two specific MMP-generated cleavage site within COL4A3. The level of fibrinogen was previously assessed in year 1 plasma. RESULTS: In COPD subjects, plasma C4Ma3 levels were significantly correlated with plasma fibrinogen levels (0.389 (P < 0.0001)). Cox proportional-hazards regression adjusted for relevant confounders showed that high levels of plasma C4Ma3, but not TUM, were related to a higher risk of mortality (hazard ratio 5.12 (95% CI 2.28-11.50), P < 0.0001). High levels of plasma fibrinogen were not associated with all-cause mortality in this subpopulation, contradictory to published results. Whereas plasma C4Ma3 multiplied by fibrinogen showed to be related to a higher risk of mortality (hazard ratio 5.74 (95% CI 2.65-12.41), P < 0.0001). Plasma C4Ma3 levels were related to the number of hospitalizations due to COPD exacerbations in the year before study start (P = 0.0375). Fibrinogen levels were related to hospitalized exacerbations prior to study start (P = 0.0058) and were also related to future exacerbations (P < 0.0001). CONCLUSION: We compared herein fibrinogen, C4Ma3 and TUM as biomarkers for COPD prognosis. Fibrinogen was related to future exacerbation, whereas C4Ma3 and the combination of C4Ma3 with fibrinogen were superior to fibrinogen alone in predicting mortality. This pilot study suggests that the assessment of plasma C4Ma3 could be important for identifying COPD patients with a poor prognosis. TRIAL REGISTRATION: NCT00292552 , GSK Study No. SCO104960.


Assuntos
Autoantígenos/sangue , Colágeno Tipo IV/sangue , Fibrinogênio/metabolismo , Doença Pulmonar Obstrutiva Crônica/sangue , Doença Pulmonar Obstrutiva Crônica/mortalidade , Idoso , Biomarcadores/sangue , Estudos de Coortes , Feminino , Hospitalização/tendências , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Mortalidade/tendências , Projetos Piloto , Prognóstico , Estudos Prospectivos , Doença Pulmonar Obstrutiva Crônica/diagnóstico
8.
Sci Rep ; 9(1): 4064, 2019 Mar 11.
Artigo em Inglês | MEDLINE | ID: mdl-30858579

RESUMO

Chronic obstructive pulmonary disease (COPD) is characterized by a slow heterogeneous progression. Therefore, improved biomarkers that can accurately identify patients with the highest likelihood of progression and therefore the ability to benefit from a given treatment, are needed. Elastin is an essential structural protein of the lungs. In this study, we investigated whether elastin degradation products generated by the enzymes proteinase 3, cathepsin G, neutrophil elastase, MMP7 or MMP9/12 were prognostic biomarkers for COPD-related outcomes. The elastin degradome was assessed in a subpopulation (n = 1307) of the Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE) cohort with 3 years of clinical follow-up. Elastin degraded by proteinase 3 could distinguish between COPD participants and non-smoking controls (p = 0.0006). A total of 30 participants (3%) died over the 3 years of observation. After adjusting for confounders, plasma levels of elastin degraded by proteinase 3 and cathepsin G were independently associated with mortality outcome with a hazard ratio per 1 SD of 1.49 (95%CI 1.24-1.80, p < 0.0001) and 1.31 (95%CI 1.10-1.57, p = 0.0029), respectively. Assessing the elastin degradome demonstrated that specific elastin degradation fragments have potential utility as biomarkers identifying subtypes of COPD patients at risk of poor prognosis and supports further exploration in confirmatory studies.

9.
Eur Respir J ; 53(5)2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30846476

RESUMO

Precision medicine is a patient-specific approach that integrates all relevant clinical, genetic and biological information in order to optimise the therapeutic benefit relative to the possibility of side-effects for each individual. Recent clinical trials have shown that higher blood eosinophil counts are associated with a greater efficacy of inhaled corticosteroids (ICSs) in chronic obstructive pulmonary disease (COPD) patients. Blood eosinophil counts are a biomarker with potential to be used in clinical practice, to help target ICS treatment with more precision in COPD patients with a history of exacerbations despite appropriate bronchodilator treatment.The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 pharmacological treatment algorithms, based on the ABCD assessment, can be applied relatively easily to treatment-naive individuals at initial presentation. However, their use is more problematic during follow-up in patients who are already on maintenance treatment. There is a need for a different system to guide COPD pharmacological management during follow-up.Recent large randomised controlled trials have provided important new information concerning the therapeutic effects of ICSs and long-acting bronchodilators on exacerbations. The new evidence regarding blood eosinophils and inhaled treatments, and the need to distinguish between initial and follow-up pharmacological management, led to changes in the GOLD pharmacological treatment recommendations. This article explains the evidence and rationale for the GOLD 2019 pharmacological treatment recommendations.

11.
J Am Coll Cardiol ; 73(17): 2166-2177, 2019 May 07.
Artigo em Inglês | MEDLINE | ID: mdl-30846341

RESUMO

BACKGROUND: The relationship between respiratory diseases and individual cardiovascular diseases, and the impact of cardiovascular diseases on mortality in patients with respiratory disease, are unclear. OBJECTIVES: This study sought to determine the relationship between chronic obstructive pulmonary disease (COPD), asthma and interstitial lung disease (ILD), and individual cardiovascular diseases, and evaluate the impact of individual cardiovascular diseases on all-cause mortality in respiratory conditions. METHODS: The authors conducted a cohort study of all patients admitted to 7 National Health Service hospitals across the North West of England, between January 1, 2000, and March 31, 2013, with relevant respiratory diagnoses, with age-matched and sex-matched control groups. RESULTS: A total of 31,646 COPD, 60,424 asthma, and 1,662 ILD patients were included. Control groups comprised 158,230, 302,120, and 8,310 patients, respectively (total follow-up 2,968,182 patient-years). COPD was independently associated with ischemic heart disease (IHD), heart failure (HF), atrial fibrillation, and peripheral vascular disease, all of which were associated with all-cause mortality (e.g., odds ratio for the association of COPD with HF: 2.18 [95% confidence interval (CI): 2.08 to 2.26]; hazard ratio for the contribution of HF to mortality in COPD: 1.65 [95% CI: 1.61 to 1.68]). Asthma was independently associated with IHD, and multiple cardiovascular diseases contributed to mortality (e.g., HF hazard ratio: 1.81 [95% CI: 1.75 to 1.87]). ILD was independently associated with IHD and HF, both of which were associated with mortality. Patients with lung disease were less likely to receive coronary revascularization. CONCLUSIONS: Lung disease is independently associated with cardiovascular diseases, particularly IHD and HF, which contribute significantly to all-cause mortality. However, patients with lung disease are less likely to receive coronary revascularization.

13.
Respir Med ; 147: 58-65, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30704700

RESUMO

BACKGROUND: SLS COPD was the first open-label randomised controlled trial demonstrating a reduction in moderate/severe COPD exacerbations with once-daily inhaled fluticasone furoate/vilanterol (FF/VI) in everyday clinical practice. Here we report FF/VI effectiveness and safety in predefined patient subgroups. METHODS: Patients with COPD, exacerbation history, and receiving maintenance inhaler therapy, were randomised to initiate FF/VI 100/25 µg or continue usual care (UC) with 12 months' follow-up. Annual rates of moderate/severe exacerbations (primary outcome), selected secondary outcomes, and incidence of pneumonia serious adverse events of special interest (SAESI) were compared between randomisation groups across various patient subgroups/baseline treatment strata. SAESI rates by actual treatment were also assessed. RESULTS: Lower exacerbation rates were observed for FF/VI versus UC across all subgroups/strata, including ICS + LABA therapy subset (8.0% [0.1, 15.4]), except in patients without baseline airflow limitation (-0.5% [-29.8, 22.1]). Larger reductions compared to the overall analysis were observed for patients on ICS-containing regimens (excluding LAMA) before the study (15.6% [3.4, 26.3]), and with baseline CAT score <10 (25.3% [-0.4, 44.4]). Pneumonia SAESI rates were similar for FF/VI versus UC across all subgroups/strata, except the LABA, LAMA or LABA + LAMA stratum (incidence ratio 2.8 [0.9, 8.5]). SAESI rates were not increased for FF/VI versus other ICS + LABA. CONCLUSIONS: Initiating FF/VI versus continuing UC reduced exacerbation rates without increased pneumonia SAESI risk compared to other ICS-containing regimens and in various patient subgroups, consistent with primary study findings. FF/VI may be a therapeutic option for a broad population of COPD patients, including those with more severe disease.

14.
Nat Genet ; 51(3): 494-505, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30804561

RESUMO

Chronic obstructive pulmonary disease (COPD) is the leading cause of respiratory mortality worldwide. Genetic risk loci provide new insights into disease pathogenesis. We performed a genome-wide association study in 35,735 cases and 222,076 controls from the UK Biobank and additional studies from the International COPD Genetics Consortium. We identified 82 loci associated with P < 5 × 10-8; 47 of these were previously described in association with either COPD or population-based measures of lung function. Of the remaining 35 new loci, 13 were associated with lung function in 79,055 individuals from the SpiroMeta consortium. Using gene expression and regulation data, we identified functional enrichment of COPD risk loci in lung tissue, smooth muscle, and several lung cell types. We found 14 COPD loci shared with either asthma or pulmonary fibrosis. COPD genetic risk loci clustered into groups based on associations with quantitative imaging features and comorbidities. Our analyses provide further support for the genetic susceptibility and heterogeneity of COPD.


Assuntos
Predisposição Genética para Doença/genética , Doença Pulmonar Obstrutiva Crônica/genética , Adulto , Idoso , Asma/genética , Estudos de Casos e Controles , Feminino , Expressão Gênica/genética , Loci Gênicos/genética , Estudo de Associação Genômica Ampla/métodos , Humanos , Pulmão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Fenótipo , Polimorfismo de Nucleotídeo Único/genética , Fibrose Pulmonar/genética , Fumar/genética
15.
Int J Chron Obstruct Pulmon Dis ; 13: 3485-3492, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30498338

RESUMO

Purpose: The changes in grading of disease severity and treatment recommendations for patients with COPD in the 2017 GOLD strategy may present an opportunity for reducing treatment burden for the patients and costs to the health care system. The aim of this study was to assess the implications of the GOLD 2017 grading system in terms of change in distribution across GOLD groups A-D for existing patients in UK primary care and estimate the potential cost savings of implementing GOLD 2017 treatment recommendations in UK primary care. Patients and methods: Using electronic health record data from the Clinical Practice Research Datalink (CPRD), patients aged ≥35 years with spirometry-confirmed COPD, receiving care during 2016, were included. The cohort was graded according to the GOLD 2017 groups (A-D), and treatment costs were calculated, according to corresponding recommendations, to observe the difference in actual vs predicted costs. Results: When applying GOLD 2013 criteria, less than half of the cohort (46%) was assigned to GOLD A or B, as compared to 86% when applying the GOLD 2017 grading. The actual mean annual maintenance treatment cost was £542 per patient vs a predicted £389 for treatment according to the 2017 GOLD strategy. Conclusion: There is a potential to make significant cost savings by implementing the grading and treatment recommendations from the 2017 GOLD strategy.

16.
Int J Chron Obstruct Pulmon Dis ; 13: 3885-3894, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30568440

RESUMO

Background: In COPD disturbed sleep is related to exacerbation frequency, poor quality of life, and early mortality. We developed the Manchester Respiratory-related Sleep Symptoms scale (MaRSS) to assess sleep-time symptoms in COPD. Methods: Focus groups including COPD and age-matched controls were used to develop an item-list, which was then administered to COPD patients and age-matched controls in a cross-sectional study. Hierarchical and Rasch analysis informed item selection and scale unidimensionality. Construct validity was examined using Pearson's correlation with the Sleep Problems Index, St George's Respiratory Questionnaire (SGRQ), and FACIT-Fatigue scale. MaRSS change scores from baseline (stable) to exacerbation were assessed in a separate sub-study of COPD patients. Results: Thirty-six COPD patients and nine age-matched controls produced an initial 26-item list. The cross-sectional study involved 203 COPD patients (male: 63%, mean age 64.7 years) and 50 age-matched controls (male: 56%, mean age 65.8 years). Eighteen items were removed to develop an eight-item unidimensional scale covering breathlessness, chest tightness, cough, sputum production, lack of sleep, and medication use. MaRSS scores significantly correlated with sleep problems, SGRQ Total, and FACIT-Fatigue (r=0.58-0.62) and demonstrated a good fit to the Rasch model (chi-squared=29.2; P=0.04). In the substudy, MaRSS scores demonstrated a moderate effect size from baseline to exacerbation visit in 27 patients with 32 exacerbation episodes (Cohen's d=0.6). Conclusion: The MaRSS is a reliable, valid, and clinically responsive measure of respiratory-related symptoms that disturb sleep. It is simple to use and score, making it suitable for research and clinical practice.


Assuntos
Pulmão/fisiopatologia , Medidas de Resultados Relatados pelo Paciente , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Respiração , Transtornos do Sono-Vigília/diagnóstico , Sono , Idoso , Estudos de Casos e Controles , Estudos Transversais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Psicometria , Doença Pulmonar Obstrutiva Crônica/complicações , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Reprodutibilidade dos Testes , Transtornos do Sono-Vigília/etiologia , Transtornos do Sono-Vigília/fisiopatologia
17.
Int J Chron Obstruct Pulmon Dis ; 13: 3997-4003, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30587955

RESUMO

Purpose: It is a challenge to control oxygen saturation (SpO2) in patients with exacerbations of COPD during admission. We tested a newly developed closed-loop system, O2matic®, and its ability to keep SpO2 within a specified interval compared with manual control by nursing staff. Patients and methods: We conducted a crossover trial with patients admitted with an exacerbation of COPD and hypoxemia (SpO2 ≤88% on room air). Patients were monitored with continuous measurement of SpO2. In random order, they had 4 hours with manually controlled oxygen and 4 hours with oxygen delivery controlled by O2matic. Primary outcome was time within a prespecified SpO2 target interval. Secondary outcomes were time with SpO2 <85%, time with SpO2 below target but not <85%, and time with SpO2 above target. Results: Twenty patients were randomized and 19 completed the study. Mean age was 72.4 years and mean FEV1 was 0.72 L (33% of predicted). Patients with O2matic-controlled treatment were within the SpO2 target interval in 85.1% of the time vs 46.6% with manually controlled treatment (P<0.001). Time with SpO2 <85% was 1.3% with O2matic and 17.9% with manual control (P=0.01). Time with SpO2 below target but not <85% was 9.0% with O2matic and 25.0% with manual control (P=0.002). Time with SpO2 above target was not significantly different between treatments (4.6% vs 10.5%, P=0.2). Patients expressed high confidence and a sense of safety with automatic oxygen delivery. Conclusion: O2matic was able to effectively control SpO2 for patients admitted with an exacerbation of COPD. O2matic was significantly better than manual control to maintain SpO2 within target interval and to reduce time with unintended hypoxemia.


Assuntos
Pulmão/fisiopatologia , Oxigenoterapia/instrumentação , Admissão do Paciente , Doença Pulmonar Obstrutiva Crônica/terapia , Idoso , Idoso de 80 Anos ou mais , Automação , Estudos Cross-Over , Dinamarca , Progressão da Doença , Desenho de Equipamento , Feminino , Volume Expiratório Forçado , Humanos , Masculino , Pessoa de Meia-Idade , Oximetria , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Fatores de Tempo , Resultado do Tratamento
19.
Int J Chron Obstruct Pulmon Dis ; 13: 3321-3330, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30349236

RESUMO

Objectives: Cardiovascular disease is often associated with COPD. Lung density quantification of images obtained from cardiac computed tomography (CT) scans would allow simultaneous evaluation of emphysema and coronary artery calcification score and provide further mechanistic insight into the relationship between these syndromes. Patients and methods: We assessed the agreement between lung density indices obtained by cardiac and full-lung CT scans. Paired cardiac and chest CT scans were assessed in 156 individuals with and without airflow limitation. Quantitative threshold indices of low attenuation area (LAA) and 15th percentile density index (PD15) were compared in terms of precision using Spearman's correlation coefficient, accuracy using concordance correlation coefficient (CCC), and relative accuracy using P15 and P30. We also assessed the relationship between visually and quantitatively determined emphysema and used receiver operating characteristic curves to evaluate the ability of lung density indices to discriminate airflow limitation. Results: Correlation coefficients between lung density indices obtained from cardiac and chest CT scans were 0.49 for percent LAA (%LAA)-950 and 0.71 for PD15. Corresponding values for CCC, P15, and P30 were 0.33, 3.2, and 5.1, respectively, for %LAA-950, and 0.34, 17.3, and 37.8, respectively, for PD15. For both cardiac and chest CT scans, visually determined emphysema was associated with higher %LAA-950 and lower PD15, and the ability of %LAA-950 and PD15 to discriminate airflow limitation were comparable. Conclusion: Although chest CT imaging is preferable, cardiac CT imaging may also be used for lung emphysema quantification where association measures are of primary interest.

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