Global mortality and readmission rates following COPD exacerbation-related hospitalisation: a meta-analysis of 65 945 individual patients

\ua9 2024, European Respiratory Society. All rights reserved.Background Exacerbations of COPD (ECOPD) have a major impact on patients and healthcare systems across the world. Precise estimates of the global burden of ECOPD on mortality and hospital readmission are needed to inform policy makers and aid preventive strategies to mitigate this burden. The aims of the present study were to explore global in-hospital mortality, post-discharge mortality and hospital readmission rates after ECOPD-related hospitalisation using an individual patient data meta-analysis (IPDMA) design. Methods A systematic review was performed identifying studies that reported in-hospital mortality, postdischarge mortality and hospital readmission rates following ECOPD-related hospitalisation. Data analyses were conducted using a one-stage random-effects meta-analysis model. This study was conducted and reported in accordance with the PRISMA-IPD statement. Results Data of 65 945 individual patients with COPD were analysed. The pooled in-hospital mortality rate was 6.2%, pooled 30-, 90- and 365-day post-discharge mortality rates were 1.8%, 5.5% and 10.9%, respectively, and pooled 30-, 90- and 365-day hospital readmission rates were 7.1%, 12.6% and 32.1%, respectively, with noticeable variability between studies and countries. Strongest predictors of mortality and hospital readmission included noninvasive mechanical ventilation and a history of two or more ECOPD-related hospitalisation

Unmet needs in the management of exacerbations of chronic obstructive pulmonary disease

Exacerbations of chronic obstructive pulmonary disease (COPD) are episodes of acute worsening of respiratory symptoms that require additional therapy. These events play a pivotal role in the natural course of the disease and are associated with a progressive decline in lung function, reduced health status, a low physical activity level, tremendous health care costs, and increased mortality. Although most exacerbations have an infectious origin, the underlying mechanisms are heterogeneous and specific predictors of their occurrence in individual patients are currently unknown. Accurate prediction and early diagnosis of exacerbations is essential to develop novel targets for prevention and personalized treatments to reduce the impact of these events. Several potential biomarkers have previously been studied, these however lack specificity, accuracy and do not add value to the available clinical predictors. At present, microbial composition and host-microbiome interactions in the lung are increasingly recognized for their role in affecting the susceptibility to exacerbations, and may steer towards a novel direction in the management of COPD exacerbations. This narrative review describes the current challenges and unmet needs in the management of acute exacerbations of COPD. Exacerbation triggers, biological clusters, current treatment strategies, and their limitations, previously studied biomarkers and prediction tools, the lung microbiome and its role in COPD exacerbations as well as future directions are discussed

Alterations in plasma hyaluronic acid in patients with clinically stable COPD versus (non)smoking controls

Hyaluronic acid (HA) is a key component of the extracellular matrix. HA and its metabolism are suggested to be altered in the lungs of patients with chronic obstructive pulmonary disease (COPD). The present study explored systemic HA, and its metabolic regulators, in patients with clinically stable COPD and smoking and non-smoking controls. Furthermore, associations of HA with acute exacerbations (AECOPD), airway-related hospitalizations, systemic inflammation and cardiovascular risk were studied. In total, 192 patients with moderate to very severe COPD [aged 62.3 y (+/- SD 7.0)], 84 smoking controls [aged 61.8 y (+/- 5.7)], and 107 non-smoking controls [aged 60.1 y (+/- 7.0)] were included. Plasma HA was reduced in patients with COPD compared to non-smoking controls (p=0.033), but was comparable after adjusting for age and sex. Expression of HAS-3 did not differ between groups, but was substantially less detectable in more patients with COPD than (non)smoking controls (p<0.001). Expression of HYAL-2 was enhanced in patients with COPD versus smoking (p=0.019) and non-smoking (p<0.001) controls, also in the age- and sex- adjusted model (p<0.001). Plasma HA was not associated with AECOPD, airway-related hospitalizations in the previous year, or systemic inflammation in COPD. Arterial pulse wave velocity explained some of the variance (<10%) in plasma HA (p=0.006). Overall, these results indicate that expression of HYAL-2, but not plasma HA nor HAS-3, is enhanced in patients with COPD compared to (non)smoking controls. Furthermore, HA was not associated with clinical outcomes, yet, cardiovascular risk might play a role in its systemic regulation in stable COPD