Background: COPD is one of the leading causes of morbidity and mortality in the world; however, the most varied amounts of clinical and laboratory characteristics acts in different ways in the mortality among over time. Therefore, this study aimed to evaluate the predictors of mortality in patients with COPD after 9 years. Patients and methods: One hundred and thirty-three patients with COPD were assessed at baseline by spirometry, pulse oximetry (SpO₂), body composition, intensity of dyspnea, distance walked in the 6-minute walk test (6MWT), and Charlson Comorbidity Index (CCI). Results: After 9 years, it was not possible to identify the lifetime of 4 patients who died and of 19 patients who stopped follow-up; thus, 110 patients were included in the analysis of predictors of mortality (67% male, 65±9 years old, and FEV₁: 52.5 [40%–73%]). Male sex, age, SpO₂, Body mass index, airway Obstruction, Dyspnea, and Exercise capacity (BODE) index, and frequency of exacerbations in the first 3 years of follow-up were considered in the model. Patients classified at baseline with BODE class 2 (HR: 2.62, 95% CI: 1.36–5.04; P=0.004), BODE class 3 (HR: 2.54, 95% CI: 1.15–5.61; P=0.02), and BODE class 4 (HR: 15.35, 95% CI: 3.11–75.75; P=0.001) showed increased risk of death compared to those with BODE class 1. The CCI (HR: 1.29, 95% CI: 1.00–1.68; P=0.04) and the number of exacerbations in the first 3 years (HR: 1.32, 95% CI: 1.00–1.76; P=0.04) also showed increased risk of death. By replacing the BODE index for the variables that compose it, those with body mass index ≤21 kg/m² showed increased risk of death compared to those with body mass index (BMI)>21 kg/m² (HR: 2.70, 95% CI: 1.38–5.25; P=0.003). Conclusion: After 9 years, we identified that those with high BODE index, greater CCI, greater frequency of exacerbations in the first 3 years, and BMI ≤21 kg/m² showed increased risk of death.

Background: Many countries have experienced 2 predominant waves of COVID-19–related hospitalizations. Comparing the clinical trajectories of patients hospitalized in separate waves of the pandemic enables further understanding of the evolving epidemiology, pathophysiology, and health care dynamics of the COVID-19 pandemic. Objective: In this retrospective cohort study, we analyzed electronic health record (EHR) data from patients with SARS-CoV-2 infections hospitalized in participating health care systems representing 315 hospitals across 6 countries. We compared hospitalization rates, severe COVID-19 risk, and mean laboratory values between patients hospitalized during the first and second waves of the pandemic. Methods: Using a federated approach, each participating health care system extracted patient-level clinical data on their first and second wave cohorts and submitted aggregated data to the central site. Data quality control steps were adopted at the central site to correct for implausible values and harmonize units. Statistical analyses were performed by computing individual health care system effect sizes and synthesizing these using random effect meta-analyses to account for heterogeneity. We focused the laboratory analysis on C-reactive protein (CRP), ferritin, fibrinogen, procalcitonin, D-dimer, and creatinine based on their reported associations with severe COVID-19. Results: Data were available for 79,613 patients, of which 32,467 were hospitalized in the first wave and 47,146 in the second wave. The prevalence of male patients and patients aged 50 to 69 years decreased significantly between the first and second waves. Patients hospitalized in the second wave had a 9.9% reduction in the risk of severe COVID-19 compared to patients hospitalized in the first wave (95% CI 8.5%-11.3%). Demographic subgroup analyses indicated that patients aged 26 to 49 years and 50 to 69 years; male and female patients; and black patients had significantly lower risk for severe disease in the second wave than in the first wave. At admission, the mean values of CRP were significantly lower in the second wave than in the first wave. On the seventh hospital day, the mean values of CRP, ferritin, fibrinogen, and procalcitonin were significantly lower in the second wave than in the first wave. In general, countries exhibited variable changes in laboratory testing rates from the first to the second wave. At admission, there was a significantly higher testing rate for D-dimer in France, Germany, and Spain. Conclusions: Patients hospitalized in the second wave were at significantly lower risk for severe COVID-19. This corresponded to mean laboratory values in the second wave that were more likely to be in typical physiological ranges on the seventh hospital day compared to the first wave. Our federated approach demonstrated the feasibility and power of harmonizing heterogeneous EHR data from multiple international health care systems to rapidly conduct large-scale studies to characterize how COVID-19 clinical trajectories evolve.

Background: Eosinophil counts increase during chronic obstructive pulmonary disease (COPD) exacerbation and influence the response to different agents (such as inhaled and systemic corticosteroids), as well as increase the production of other inflammatory cytokines. However, few studies have evaluated the association between peripheral blood eosinophils with mortality rate. Objective: To evaluate the association between peripheral blood eosinophils and mortality rate in COPD patients over a nine-year period. Study Design and Methods: This cohort included 133 COPD patients assessed at baseline by spirometry, pulse oximetry (SpO₂), complete blood count, body composition, dyspnea intensity [Modified Medical Research Council (mMRC)] and the six-minute distance test (6MWD). The Kaplan–Meier curve followed by a Log rank test was used to evaluate mortality rate related to eosinophil cutoff point categorization. Multivariate Cox regression analysis was performed to identify the association between eosinophils and mortality with all subjects evaluated at baseline, adjusted for age, gender, mMRC, 6MWT, forced expiratory volume in the first second (FEV₁) and SpO₂. Results: Nineteen patients did not complete follow-up and it was not possible to identify the date of death in four others. Therefore, 110 patients were included in the analysis. At baseline, 81% presented ≥ 150 eosinophil cells and 72% presented ≥ 2%. We identified a three-fold higher risk of death in those with < 2% eosinophils and < 150 cells. We did not identify statistical differences when using other cutoff points. Conclusion: The decrease in number of peripheral eosinophils, with cutoff points at 2% and 150 cells, may be associated with a higher risk of death in COPD patients over nine years.

Background/Objectives: Post-COVID-19 condition can manifest through various symptoms such as dyspnea, cognitive disturbances, and fatigue, with mechanisms related to these symptoms, particularly those related to fatigue, still requiring further clarification. Therefore, our aim was to assess the clinical and physiological variables in patients with post-COVID-19 condition and persistent fatigue. Methods: After one year post-COVID-19 infection, the patients underwent a comprehensive evaluation, including a complete blood count, a metabolic panel, complete spirometry, and assessments of dyspnea, quality of life, anxiety and depression, physical capacity, body composition, muscle strength, comorbidities, and medications. The participants were categorized into two groups: G1—fatigue and G2—non-fatigue. Results: Seventy-seven patients (53% female; 55 ± 11.8 years) were included, 37 in G1 and 40 in G2. As for clinical markers and symptoms of illness, in those with persistent fatigue symptoms, a greater sensation of dyspnea [BDI score: 7.5 (6–9) vs. 12 (9–12), p < 0.001; mMRC score: 1 (1–2) vs. 0 (0–1), p = 0.002], worse quality of life [SGRQ total score: 1404 (1007–1897) vs. 497 (274–985); p < 0.001], higher levels of anxiety [HADS-A score: 8 (5–9) vs. 3 (0.5–4); p < 0.001], and a reduction in peripheral and inspiratory muscle strength [handgrip strength: 34 (28–40) vs. 40 (30–46.5) kgf, p = 0.044; MIP: −81 ± 31 vs. −111 ± 33 mmHg, p < 0.001)] were observed. Conclusions: Those with persistent fatigue exhibited a greater sensation of dyspnea, higher levels of anxiety, reduced peripheral and inspiratory muscle strength, and a greater impairment of quality of life. The severity of fatigue was influenced by the worsening quality of life, heightened anxiety levels, and decreased peripheral muscle strength. Additionally, the worse quality of life was associated with a higher sensation of dyspnea, lower muscle strength, and reduced physical capacity.

This brief communication demonstrates the correlation of persistent respiratory symptoms with functional, tomographic, and transbronchial pulmonary biopsy findings in patients with COVID-19 who had a long follow-up period. We report a series of six COVID-19 patients with pulmonary involvement who presented with persistent dyspnea within 4-15 months of discharge. We performed transbronchial biopsies, and the histopathological pattern consistently demonstrated peribronchial remodeling with interstitial pulmonary fibrosis. Therefore, lung biopsy may be useful in the approach of patients with long COVID-19, although the type of procedure, its precise indication, and the moment to perform it are yet to be clarified. (Brazilian Registry of Clinical Trials-ReBEC; identifier: RBR-8j9kqy [http://www.ensaiosclinicos.gov.br])

Background: Systemic manifestations of chronic obstructive pulmonary disease (COPD) are related to increased systemic inflammatory process; however, it is not entirely clear how much they are related and how the systemic inflammation, in particular interleukin-6 (IL-6), is associated with exacerbation and mortality risk. Objective: To evaluate the role of IL-6 in COPD patients over nine years. Study Design and Methods: A total of 133 COPD patients were assessed at baseline between 2004 and 2006 and reassessed after three and nine years through clinical evaluation, comorbidities, hematological blood count and IL-6 analysis. Results: After nine years, 19 patients lost the follow-up and were not possible to identify the date of death of four patients; 12 refused to participate and 1 could not be involved due to recurrent exacerbations. Therefore, 33 patients were included in the reassessment after nine years of follow-up and 92 patients were included in the Cox mortality analysis with IL-6 as a time-dependent covariate. Regarding the inflammatory profile, in patients who survived after nine years, there was a significant increase in IL-6 [0.4 (0.2– 0.8) vs 5.7 (3.4– 11) pg/mL; p < 0.001] and reduction in lymphocyte count [2.1 (1.6– 2.4) vs 1.4 (1.2– 2.1)10^9/L; p < 0.01] with an increase in the neutrophil/lymphocyte ratio (2.0 ± 0.7 vs 2.7 ± 1.2; p = 0.003). The Cox mortality model did not show a statistical significance influence of IL-6 assessed during the follow-up. Conclusion: There was a progressive increase in IL-6 during the follow-up, however, without influence on mortality.