Chronic Obstructive Pulmonary Diseases-Journal of the Copd Foundation最新文献

Background: Nontuberculous mycobacteria pulmonary disease (NTM-PD) is an emerging public health concern with increasing incidence and prevalence. Despite its chronic and progressive nature, there is a notable gap in research on the factors influencing hospital outcomes in this patient population.

Materials and methods: We conducted a retrospective cohort study using data from the National Inpatient Sample (NIS) to analyze hospitalizations of adult patients diagnosed with NTM-PD. We examined patient demographics, comorbidities, and hospital characteristics to identify predictors of hospital length of stay (LOS) and discharge disposition. Multivariate negative binomial regression and logistic regression models were employed to assess the impact of these variables.

Results: The study included 1167 hospitalized NTM-PD patients, with a mean age of 66.9 years. The overall mean LOS was 7.4 days, with an average hospital cost of $15,606. Discharge to a nursing home was associated with a 78% longer LOS (incidence rate ratio=1.78, p<0.0001). Key predictors of extended LOS included male gender, private insurance status, higher comorbidity burden, and increased number of procedures. Patients discharged to nursing homes were more likely to be older males with complex medical profiles. Interestingly, conditions such as malignancy and COPD, while linked to longer LOS, were associated with a decreased likelihood of discharge to a nursing home.

Conclusion: Our study highlights significant predictors of LOS and discharge outcomes in NTM-PD patients, emphasizing the need for personalized and proactive management. These findings underscore the importance of targeted interventions in the outpatient setting to reduce hospital admissions and improve patient outcomes.

Background: The objective of this study was to construct a prediction model to assess the onset of acute heart failure (AHF) in patients with chronic obstructive pulmonary disease (COPD) without a history of heart failure and to evaluate the predictive value of the nomogram.

Methods: This study involved 3730 patients with COPD and no history of heart failure. Clinical and laboratory data were collected from the Medical Information Mart for Intensive Care IV database. The patients were divided into a training set (2611 cases) and a validation set (1119 cases) in a 7:3 ratio. Least absolute shrinkage and selection operator (LASSO) regression was used to identify potential risk factors for AHF in patients with COPD. These factors were then subjected to multivariate logistic regression analysis to develop a prediction model for the risk of AHF. The model's differentiation, consistency, and clinical applicability were evaluated using receiver operating characteristic analysis, a calibration curve, and decision curve analysis (DCA), respectively.

Results: LASSO regression identified 10 potential predictors. The concordance index was 0.820. The areas under the curves for the training and validation sets were 0.8195 and 0.8035, respectively. The calibration curve demonstrated strong concordance between the nomogram's predictions and the actual outcomes. DCA confirmed the clinical applicability of the nomogram.

Conclusion: Our nomogram is a reliable and convenient tool for predicting acute heart failure in patients with COPD.

Background: Pseudomonas aeruginosa is an important pathogen in patients with chronic respiratory diseases. It can colonize the airways and could have prognostic value in bronchiectasis and cystic fibrosis. Its role in chronic obstructive pulmonary disease (COPD) is less well-defined.

Methods: A prospective study was conducted in Hong Kong to investigate the possible association between Pseudomonas aeruginosa colonization and acute exacerbation of COPD (AECOPD) risks.

Results: Among 327 Chinese patients with COPD, 33 (10.1%) of the patients had Pseudomonas aeruginosa colonization. Patients with or without Pseudomonas aeruginosa colonization had similar background characteristics. Patients with Pseudomonas aeruginosa colonization had increased risks of moderate to severe AECOPD, severe AECOPD, and pneumonia with an adjusted odds ratio (aOR) of 3.15 (95% CI 1.05-9.48, p=0.042), 2.59 (95% CI 1.01₋6.64, p=0.048), and 4.19 (95% CI 1.40₋12.54, p=0.011) respectively. Patients with Pseudomonas aeruginosa colonization also had increased annual frequency of moderate to severe AECOPDs, median 0 (0₋0.93) in the non-Pseudomonas aeruginosa colonization group and 1.35 (0₋3.39) in the Pseudomonas aeruginosa colonization group, with a p-value of 0.005 in multivariate linear regression.

Conclusion: Pseudomonas aeruginosa colonization is a potential independent risk factor for moderate to severe AECOPD and pneumonia among patients with COPD without coexisting bronchiectasis.

Background: Chronic bronchitis (CB), classically defined as having cough and sputum production for at least 3 months per year for 2 consecutive years, is frequently associated with chronic obstructive pulmonary disease (COPD).

Methods: This retrospective cohort study using the Optum^® de-identified electronic health record data set (Optum^® EHR) aimed to identify patients with CB, COPD, and both CB and COPD through the application of the classical definition of CB, and to compare the characteristics of these populations, and the timing of diagnosis as well as their health care resource utilization (HCRU). Scanning of the EHRs was performed electronically using a specially developed algorithm.

Results: Of 104,633,876 patients in the study period between January 2007 and September 2020, 628,545 patients had CB only (i.e., nonobstructive disease), 129,084 had COPD only (COPD cohort), and 77,749 had both COPD and CB (COPD-CB cohort). A total of 75.9% of patients (59,009 of 77,749) fulfilled the criteria for a CB diagnosis before their first diagnosis with COPD, compared with 24.1% who had COPD before being diagnosed with CB. HCRU over 5 years was highest in the COPD-CB cohort, whereas the COPD cohort and CB cohorts had similar HCRU over 5 years. The COPD-CB cohort had a greater percentage of common COPD comorbidities and exposure to more drug classes than the other cohorts.

Conclusions: These results highlight the importance of increased attention to CB. CB often precedes the diagnosis of COPD and subsequently leads to high HCRU. Interventions to better manage CB and prevent the progression of CB to COPD could improve morbidity in this population.

Objective: The severity of emphysema may be measured by lung density on computed tomography (CT) scanning, and in alpha-1 antitrypsin deficiency (AATD) this measure has been used as the primary outcome in trials of disease-modifying therapy, namely augmentation. However, the minimum clinically important difference (MCID) in lung density change is not known; this study aimed to derive and validate MCIDs for density values in AATD.

Methods: The distribution method and anchoring density against forced expiratory volume in 1 second (FEV₁) were used to derive mean and 95% confidence intervals for the MCID. Data from systematic reviews of CT density measurement and therapy for AATD obtained both absolute and annual changes in lung density. Using the range of potential MCID generated by these methods, a value was chosen for validation against mortality, lung function, and health status in the Birmingham, United Kingdom AATD cohort, using regression to adjust for confounders.

Results: Anchor and distribution methods generated a probable MCID of -1.87 g/L/year (range -1.53 to -2.20). The greatest differences between groups were found at the -2.2g/L/year with a greater FEV₁ decline in individuals with greater lung loss. Absolute lung density change had a probable MCID of -2.04g/L (range -1.83 to -2.30), and there was a difference in lung function (p<0.001) and mortality; where individuals whose absolute lung loss of more than -2.04g/L had a greater risk of death (p<0.05).

Interpretation: From initial evidence, we have shown absolute lung density change as a potential outcome for emphysema modifying therapies in AATD rather than annual density change, with an MCID of -2.04g/L.

Introduction: Chronic obstructive pulmonary disease (COPD) poses a substantial burden on individuals and the U.S. health care system. Up-to-date information describing individuals with COPD and their acute hospital-based health care utilization at the state level and by insurance type is lacking.

Methods: Individuals with COPD aged 40 and older were identified from large databases of Medicare fee-for-service, Medicaid, and commercial health insurance claims, and counts were extrapolated to the U.S. health insurance market. Demographics and outcome metrics were quantified between January 1 and December 31, 2021, and summarized by state and insurance type.

Results: Approximately 11.7 million insured individuals had COPD in 2021. The largest share were covered by Medicare (79.4%), followed by commercial insurance (11.3%) and Medicaid (9.3%). COPD prevalence varied among states, ranging from 44 (Utah) to 143 (West Virginia) per 1000 insured individuals. Nationwide, annual all-cause mortality for individuals with COPD covered by Medicare (11.5%) was more than double that of Medicaid (5.1%). There were 1.8 million COPD-related acute inpatient hospitalizations nationwide, with the largest share among individuals covered by Medicare (86.4%), followed by Medicaid (9.0%) and commercial insurance (4.6%). COPD-related hospitalization rates also varied among states, ranging from 97 (Idaho) to 200 (District of Columbia) per 1000 individuals with COPD. There were 1.4 million COPD-related emergency department/observation encounters not resulting in acute inpatient admissions nationwide.

Conclusion: There is substantial state and payer variation in COPD prevalence and burden. Understanding this variation provides valuable insights into populations with unmet needs that can inform public health strategies to address gaps.

Background: Alpha-1 antitrypsin (AAT) deficiency is the most common genetic cause of emphysema. Chymotrypsin-like elastase 1 (CELA1) is a serine protease neutralized by AAT and is important in emphysema progression. Cela1-deficiency is protective in murine models of AAT-deficient emphysema. KF4 anti-CELA1 antibody prevented emphysema in porcine pancreatic elastase (PPE) and cigarette smoke models in wild-type mice.

Methods: We evaluated potential toxicities of KF4 and its ability to prevent emphysema in AAT deficiency. We found Cela1 protein expression in mouse lungs, pancreas, small intestine, spleen, and bone marrow. In toxicity studies, mice treated with KF4 25mg/kg weekly for 4 weeks showed an elevation in blood urea nitrogen and slower weight gain compared to lower doses or equivalent dose immunoglobin G (IgG). By histologic grading of tissue injury of the lung, kidney, liver, and heart, there was some evidence of liver injury with KF4 25mg/kg, but in all tissues, injury was less than in control mice subjected to cecal ligation and puncture. In efficacy studies, KF4 doses as low as 0.5mg/kg reduced the lung elastase activity of AAT^-/- mice treated with 0.2 units of PPE.

Results: In this injury model, AAT^-/- mice treated with KF4 1mg/kg weekly, human purified AAT 60mg/kg weekly, and combined KF4 and AAT treatment had less emphysema than mice treated with IgG 1mg/kg weekly. However, the efficacy of KF4, AAT, or KF4 and AAT was similar.

Conclusion: While KF4 might be an alternative to AAT replacement, combined KF4 and AAT replacement does not confer additional benefit.

Background: Cigarette smoke contributes to skeletal muscle wasting. While exercise and nutritional therapies are effective in improving skeletal muscle quantity and quality, the effect of medications on longitudinal muscle loss is unclear. We investigated whether long-term use of common medications affects longitudinal skeletal muscle changes in current and former smokers.

Methods: Using quantitative computed tomography imaging, we measured the 5-year changes in pectoralis muscle area (delta-PMA) and pectoralis muscle density (delta-PMD) of 4191 participants in the COPD Genetic Epidemiology (COPDGene^®) study. We tested whether specific medications were associated with delta-PMA and/or delta-PMD using regression analyses. Propensity score matching (PSM) analysis was performed to determine the effect of the medications on longitudinal changes on delta-PMA.

Results: Over the study period, the median delta-PMA for the entire population showed a decrease of 2.23cm² (interquartile range: -6.52, 1.54). Regression analyses demonstrated statin use was associated with less loss of PMA, whereas, aspirin use was associated with a greater loss of PMA. Specifically, in the PSM-adjusted analysis, statin use was associated with attenuated loss of PMA (median; -1.5 versus -2.5cm², p=0.017), while aspirin use was associated with increased loss of PMA (median; -2.5 versus -1.9cm², p=0.040).

Conclusion: In current and former smokers, statin use was associated with reduced pectoralis muscle wasting, while aspirin use was associated with increased muscle loss. Additional research is needed to verify these findings. (Clinicaltrials.gov identifier NCT00608764).

Objective: Chronic obstructive pulmonary disease (COPD) is closely associated with arthritis. This study aims to evaluate the correlation between COPD and mortality among participants with arthritis.

Methods: The study included 11,298 participants from the National Health and Nutrition Examination Survey (NHANES) 1999-2018, who self-reported having arthritis. Cox proportional hazard models were used to assess the association between COPD and mortality among participants with arthritis. Kaplan-Meier survival curves were plotted to compare survival probabilities between groups. Subgroup and sensitivity analyses were conducted to assess the robustness of the results.

Results: During an average follow-up of 8.8 years, 3061 all-cause deaths were observed, including 1024 related to cardiovascular disease (CVD). After weighted multivariable adjustment, COPD was found to be significantly associated with both all-cause and CVD mortality among these arthritis participants. The hazard ratio (HR) for all-cause mortality among arthritis patients with COPD was 1.41 (95% confidence interval [CI]: 1.25-1.60, p < 0.001), and the HR for CVD mortality was 1.29 (95% CI: 1.08-1.53, p < 0.001). Kaplan-Meier survival curves attributed higher rates of both all-cause and CVD mortality among participants with COPD compared to those without (log-rank test, p < 0.001). Additionally, COPD increased the risk of both chronic lower respiratory disease (CLRD) mortality (HR 5.46, 95% CI: 3.48-8.56, p < 0.001) and non-CLRD mortality (HR 1.24, 95% CI: 1.07-1.44, p=0.004).

Conclusion: In the American population, arthritis patients with COPD have higher risks of all-cause and CVD mortality compared to those without COPD.