Predictors of health status do not change over three-year periods and exacerbation makes difference in chronic obstructive pulmonary disease

<p>Abstract</p> <p>Background</p> <p>The association between disease markers and health status (HS) overtime is unclear. The aim of this study was to verify the predictors of HS at baseline and after three years in Chronic Obstructive Pulmonary Disease (COPD) patients.</p> <p>Methods</p> <p>Ninety-five consecutive COPD patients (66% male, age = 67 ± 9 y, FEV₁= 58 ± 23%) underwent the following evaluations at baseline and after three years: body composition, pulse oximetry (SpO₂), six-minute walk distance (6MWD), Modified edical Research Council dyspnea scale (MMRC) and Saint George's Respiratory Questionnaire (SGRQ). The Charlson comorbidity index and BODE index were calculated. COPD exacerbations during the follow-up were evaluated. At baseline, age, gender, smoking, SpO₂, BODE index or its components (BMI, MMRC, FEV₁and 6MWD), and Charlson index were included in a multiple linear regression analysis with the baseline SGRQ total score as the dependent variable. After three years, we included the final values of the variables plus the number of exacerbations and the final SGRQ total score as the dependent variable.</p> <p>Results</p> <p>SGRQ total score (42 ± 19% <it>vs </it>44 ± 19%; p = 0.041) and activity domain (52 ± 21% <it>vs </it>60 ± 22%; p < 0.001) deteriorated during follow-up. At baseline, BODE index was selected as a predictor of SGRQ total score (R²= 0.46; p < 0.001); after three years, BODE index and age were the predictors (R²= 0.49; p < 0.001). When the BODE index was replaced by its variables, MMRC was selected as the only variable associated with the SGRQ total score (R²= 0.58; p < 0.001). After three years, MMRC, FEV₁and number of exacerbations were selected as predictors of SGRQ total score (R²= 0.63; p < 0.001).</p> <p>Conclusion</p> <p>HS deteriorated significantly over the three-year period and the predictors of HS do not change over time. BODE index and dyspnea were predictors at baseline and after three years. Exacerbation was also a predictor of HS after three years.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT00605540">NCT00605540</a></p

Smoking status and tumor necrosis factor-alpha mediated systemic inflammation in COPD patients

<p>Abstract</p> <p>Background</p> <p>Smoking cause airway and systemic inflammation and COPD patients present low grade inflammation in peripheral blood. However, data on the influence of smoking itself on systemic inflammation in COPD patients are scarce. This study investigated the association between inflammation, smoking status, and disease.</p> <p>Methods</p> <p>A cross-sectional analysis comparing 53 COPD ex-smokers, 24 COPD current smokers, 24 current smoker controls and 34 never-smoker controls was performed. Assessments included medical history, body composition, spirometry, and plasma concentration of tumor necrosis factor-alpha (TNF-α), interleukins (IL)-6, IL-8, and C-reactive protein (CRP).</p> <p>Results</p> <p>Our exploratory analysis showed that serum TNF-α was higher in COPD current smokers [4.8(4.2-5.8)pg/mL] and in current smoker controls [4.8 (4.2-6.1) pg/mL] when compared to COPD ex-smokers [4.3 (3.9-4.9)pg/mL; p = 0.02] and to never-smoker controls [3.7 (3.4-4.0)pg/mL; p < 0.001]. Multiple regression results with and without adjustment for covariates were consistent with the hypothesis that TNF-α levels were associated with smoking status in both models (p < 0.001 and p < 0.001). IL-6 and CRP were significantly higher in COPD patients when compared to smoker and never-smoker controls and the multiple regression analysis confirmed the association of these mediators with disease, but not with smoking status (p < 0.001 and p < 0.001). IL-8 had only a borderline association with disease in both models (p = 0.069 and p = 0.053). No influence of disease severity, inhaled corticosteroid, fat-free mass (FFM) depletion and long term oxygen therapy (LTOT) use on systemic inflammation was found.</p> <p>Conclusion</p> <p>Smoking may influence TNF-α mediated systemic inflammation, which, in turn, may account for some of the benefits observed in patients with COPD who stop smoking.</p

Case report: Biliobronchial fistula after biliary tract stenosis

Biliobronchial fistula (BBF) is a rare abnormality resulting from congenital or acquired communication between the bile ducts and the bronchial tree. Patients often suffer from chronic cough, dyspnea, and bilioptysis, a pathognomonic symptom of this condition. Conservative methods such as less-invasive procedures are gradually consolidating. Nonetheless, surgery remains the primary treatment, especially in more complex cases. We present the case of a 44-year-old woman with a chronic cough, no verified periods of fever, cyclic jaundice, and episodes of yellowish sputum. She had undergone cholecystectomy in 2018 and had been hospitalized several times since for pneumonia treatment. All consequent investigations for mycobacteriosis were negative. When referred to our hospital, she had cyclic jaundice and parenchymal consolidation in the right lower lobe. Suspected bilioptysis motivated the search for a biliobronchial fistula. Magnetic resonance cholangiography (MRC) confirmed stenosis of the biliary tract and fistulous path, and sputum analysis indicated high bilirubin levels. External biliary bypass was performed as an initial conservative and definitive therapy due to the presence of liver cirrhosis. Although BBF is a rare condition when bilioptysis is suspected, a diagnostic investigation should be initiated. Our case study proposes two criteria for diagnosis: an imaging exam demonstrating the fistulous path and confirmation of bilirubin in the sputum or bronchoalveolar lavage (BAL). When diagnosed, surgical correction should be performed

DElaying Disease Progression In COPD with Early Initiation of Dual Bronchodilator or Triple Inhaled PharmacoTherapy (DEPICT): A Predictive Modelling Approach (Jun, 10.1007/s12325-023-02583-1, 2023)

[No abstract available

Increased production of hydrogen peroxide by peripheral blood monocytes associated with smoking exposure intensity in smokers

<p>Abstract</p> <p>Background</p> <p>Smoking is known to be associated with oxidative stress; however, it has not been elucidated whether the oxidative response is influenced by the intensity of smoking exposure.</p> <p>Objectives</p> <p>Evaluate the effect of smoking exposure on the secretion of hydrogen peroxide (H₂O₂) by the peripheral blood monocytes of smokers.</p> <p>Methods</p> <p>A total of 25 smokers (50.3±8.8 years, 48% male) underwent the following evaluations: spirometry, pulse oximetry, body composition and total peripheral blood count. Peripheral blood monocyte (PBM) cultures were isolated and maintained, and IL-6 and TNF-α were measured in the plasma and in the supernatants of spontaneous and stimulated cultures. H₂O₂ was evaluated in the supernatants of the PBM cultures, and a subset of the PBM culture supernatants was stimulated with phorbol myristate acetate (PMA). We also evaluated 38 healthy controls (49.1±8.2 years, 42% male).</p> <p>Results</p> <p>The spontaneous and stimulated monocytes’ secretion of H₂O₂ were statistically higher in the smokers than in the healthy controls (p<0.001). The H₂O₂ secretions were statistically significant higher after stimulation with PMA in both groups (p<0.001). In the multiple regression analysis, we identified a positive, statistically significant association between pack-years of smoking and the spontaneous secretion of H₂O₂ by PBM culture, adjusted for potential confounding variables. The association between PBM culture secretion of H₂O₂ and the production of TNF-α and IL-6 was not significant.</p> <p>Conclusion</p> <p>We identified a positive association between higher production of H₂O₂ in smokers and higher smoking exposure during life. The influence of pack-years smoking may be a key modifiable factor in oxidative stress associated to smoking.</p

Effects of active smoking on airway and systemic inflammation profiles in patients with chronic obstructive pulmonary disease

Background: The markers that characterize local and systemic inflammation in chronic obstructive pulmonary disease (COPD) remain unclear, as do their correlations with smoking status and presence of disease. The aim of this study was to assess markers of inflammation in the peripheral blood and airways of current smokers without COPD, of current smokers with COPD and of ex-smokers with COPD. METHODS: In this study, 17 current smokers with COPD (mean age: 58.2 ± 9.6 years; mean forced expiratory volume in 1 second [FEV1]: 56.1 ± 15.9%), 35 ex-smokers with COPD (mean age: 66.3 ± 7.3 years; mean FEV1: 47.9 ± 17.2%) and 20 current smokers without COPD (mean age: 49.1 ± 6.2 years; mean FEV1: 106.5 ± 15.8%) were evaluated. Spirometry findings, body composition and serum/induced sputum concentrations of tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-8 and IL-10, together with serum C-reactive protein (CRP) levels, were assessed. RESULTS: Serum TNF-α concentration was higher in all current smokers than in ex-smokers with COPD. In current smokers without COPD, serum CRP level was lower than in ex-smokers with COPD and significantly lower than in current smokers with COPD. Sputum TNF-α concentration was higher in current and ex-smokers with COPD than in current smokers without COPD. Multiple regression analyses showed that serum TNF-α was associated with active smoking, and serum CRP and sputum TNF-α were associated with COPD diagnosis. CONCLUSIONS: Smoking is associated with higher systemic inflammation in patients with COPD. Current findings also support the hypothesis that smoking and COPD have different effects on the regulation of airway and systemic inflammatory processes. © 2013 Lippincott Williams and Wilkins