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Background: Exacerbation of chronic obstructive pulmonary disease (ECOPD) significantly impact health status, hospitalization rates, and disease progression, and are linked to increased mortality. Predictive factors for ECOPD are therefore of considerable interest. The limited understanding of interleukin 16 (IL-16) and IL-25 role in ECOPD provided the rationale for this study. Methods: Fifty ex-smokers diagnosed with COPD (22 ECOPD and 28 patients in the stable phase of the disease) underwent prospective analysis to evaluate the role of I IL-25 as predictive markers of clinical outcomes in ECOPD. Results: We observed a significantly lower IL-16 and higher IL-25 concentrations among ECOPD patients (p = 0.002 and p = 0.01 respectively). We also detected a significant negative correlation between IL-16 and neutrophil-to-lymphocyte ratio (NLR) (p = 0.04) and a significant negative correlation between IL-25 concentration and absolute eosinophil count (p = 0.04). In the entire group, we observed a positive correlation between IL-16 and both FEV1 and FVC, both expressed as a percentage of reference value, (p = 0.002 and p = 0.0004 respectively). However, after stratification to ECOPD and stable COPD group, significance maintained for FVC (p = 0.045 for ECOPD and p = 0.02 for stable COPD). In survival analysis, we detected significantly lower all-cause mortality for 3rd tertile of IL-16 concentrations, with a hazard ratio of 0.33 (95%CI: 0.11–0.98; p = 0.04). Conclusions: Lower IL-16 levels among ECOPD patients may indicate a feedback mechanism linked to heightened Th1 response activation. Observed correlations with ventilatory parameters and survival also seems to reflect this mechanism. The higher IL-25 concentrations observed in ECOPD patients, along with the negative correlation with absolute eosinophil count and eosinopenia, suggest multifactorial regulation and independent functions of eosinophils and IL-25. Hypothetically, this paradox may be related to the Th1/Th2 imbalance favoring Th1 response. Obtained results should be reproduced in larger size samples. [ABSTRACT FROM AUTHOR]

Introduction: Chronic obstructive lung diseases, such as asthma and COPD, appear to have a more extensive impact on overall functioning than previously believed. The latest data from clinical trials suggests a potential link between cognitive deterioration and chronic obstructive inflammatory lung disease. This raises the question of whether these diseases affect cognitive functions and whether any relevant biomarker may be identified. Methods: This prospective observational study included 78 patients divided equally into asthma, COPD, and control groups (n=26, 27 and 25 respectively). The participants underwent identical examinations at the beginning of the study and after at least 12 months. The test battery comprised 16 questionnaires (11 self-rated, 5 observer-rated, assessing cognition and mental state), spirometry, and blood samples taken for PKA and CREB mRNA evaluation. Results: A 2.3-fold increase in CREB mRNA was observed between examinations (p=0.014) for all participants; no distinctions were observed between the asthma, COPD, and control groups. Pooled, adjusted data revealed a borderline interaction between diagnosis and CREB expression in predicting MMSE (p=0.055) in COPD, CREB expression is also associated with MMSE (b=0.273, p=0.034) like with the other conducted tests (b=0.327, p=0.024) from COPD patients. No correlations were generally found for PKA, although one significant negative correlation was found between the first and second time points in the COPD group (b=-0.4157, p=0.049). Discussion: Chronic obstructive lung diseases, such as asthma and COPD, may have some linkage to impairment of cognitive functions. However, the noted rise in CREB mRNA expression might suggest a potential avenue for assessing possible changes in cognition, especially in COPD; such findings may reveal additional transcription factors linked to cognitive decline. [ABSTRACT FROM AUTHOR]

Background: Exacerbations of COPD (ECOPD) are important events in the course of COPD and they accelerate the rate of decline of lung function, and exacerbations requiring hospitalization are associated with significant mortality. Therefore, developing approaches of prevention and early treatment of ECOPDs are of special clinical interests. One of such approaches is telecare, including home telemonitoring.Material and Methods: Daily telemonitoring of HR, BP, SpO2 and spirometry was performed. Variables were compared using the bootstrap-boosted inference tests: the paired t-test or Wilcoxon signed rank test, depending on data normality, and categorical variables were compared using exact McNemar's test.Results: Nineteen patients were included to the study. We observed significant decrease in SpO2 7 days preceding ECOPD (P = 0.007; Pbootstrap-boosted = 0.005) and increase in number of events of day-to-day decrease in oxygen saturation >4% in the period of 7 days preceding ECOPD versus reference period (P = 0.02).Conclusions: Oxygen saturation telemonitoring would be successfully used in predicting ECOPD. Recording of day-to-day decrease in oxygen saturation >4% as alarming events would be effective approach which would be easily implemented in telemonitoring devices, however this outcome should be further validated in larger size samples. [ABSTRACT FROM AUTHOR]

Although current therapies in chronic obstructive pulmonary disease (COPD) improve the quality of life, they do not satisfactorily reduce disease progression or mortality. There are still many gaps in knowledge about the cellular, molecular, and genetic mechanisms contributing to pathobiology of this disease. However, increasing evidence suggests that accelerated aging, chronic systemic inflammation, and oxidative stress play major roles in pathogenesis in COPD, thus opening new opportunities in therapy. Therefore, the aim of our review was to describe and discuss some of the most widely used therapeutics that affect the root cause of aging and oxidative stress (metformin, melatonin, sirolimus, statins, vitamin D, and testosterone) in context of COPD therapy. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases play an important role in the morbidity and mortality of patients with obstructive lung diseases. Impaired vascular endothelial function seems to be a key element linking obstructive lung disease and cardiovascular disease. Recently developed technique named flow mediated skin fluorescence (FMSF) is a novel, non-invasive tool to study microvascular function. Total of 69 volunteers including 26 patients with chronic obstructive pulmonary disease (COPD), 23 patients with asthma and 20 healthy subjects underwent microvascular function assessments using FMSF. FMSF assessments were composed of measurements of reduced form of nicotinamide adenine dinucleotide (NADH) fluorescence intensity signal during brachial artery occlusion – ischemic response (IR max) and immediately after release of occlusion – hyperemic response (HR max). Associations of microvascular function with clinical and biochemical characteristics of studied subjects were also evaluated. The median value of IR max was significantly lower in COPD subjects (2.4 [1.0–6.7] %) compared with healthy subjects (9.6 [3.7–13.5] %; p < 0.01). The mean value of HR max was also significantly reduced in COPD subjects (9.7 (4.5) %) compared with both asthma subjects (12.1 (3.5) %; p < 0.05) and healthy control subjects (13.4 (2.9) %; p < 0.01). The FMSF technique makes it possible to identify impairments of the microvascular function in patients with COPD, but not in asthma patients. These exploratory findings require further validation in a larger patients cohort. • FMSF identifies impairments of the microvascular function in patients with COPD, but not in asthma patients. • FMSF appears as simple and non-invasive tool to study microcirculation and mitochondrial function. • Further studies are needed to determine the diagnostic potential of the FMSF technique. [ABSTRACT FROM AUTHOR]