scholarly journals Current data on improvement in physical tolerance and a role of physical activity in patients with chronic obstructive pulmonary disease

2019 ◽  
Vol 29 (2) ◽  
pp. 207-215
Author(s):  
Zaurbek R. Aisanov ◽  
Yuliya G. Belotserkovskaya ◽  
Sergey N. Avdeev ◽  
Andrey S. Belevskiy

Physical activity plays an important prognostic role in patients with chronic obstructive pulmonary disease (COPD). According to published data, decreased physical activity is associated with higher frequency of COPD exacerbations, higher mortality, and lower quality of life in COPD patients. As the airflow limitation is an underlying mechanism of COPD, double bronchodilators can reduce lung hyperinflation and improve exercise tolerance in patients with COPD. According to the robust evidence on the efficacy of tiotropium/olodaterol combination, double bronchodilators can increase exercise duration and time before dyspnea occurrence on exertion. However, further studies are needed in the field of rehabilitation and a role of physical activity in the management of patients with COPD.

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Ramy Karem Ali Ali ◽  
Yasser Mosafa Mohammed Mostafa ◽  
Tamer Mohammed Ali

Abstract Background Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation associated with an enhanced chronic inflammatory response in the airway, acute exacerbations of COPD can lead to progressive respiratory failure necessitating mechanical ventilation. Weaning of these patients may prove difficult and a spontaneous breath trial should be provided before the decision of extubation. Aim To evaluate the role of capnograghy in COPD patients during weaning from mechanical ventilation. Subject and methods This was a cross sectional prospective study conducted on 50 patients who were admitted at the Respiratory Intensive Care Unit of Abbassia Chest hospital and diagnosed as COPD and on mechanical ventilation. During the weaning trial, the role of capnography device evaluated considering the ability of Pet CO2 parameter in predicting hypercapnia and subsequently weaning outcome Results The changes in ABG reading before and after the SBT, PaCO2 and Pet CO2 showed significant elevation at the end of SBT,P=0.001 for both, while O2 saturation was significantly decrease at the end of SBT, P0.001. Conclusion The study found that Pa CO2 and PetCO2 are correlated to each other before, during and after SBT. Most of the studies that was found reported that PetCO2 is highly correlated with Paco2 and that PetCO2 may be a rapid and reliable predictor of arterial PaCO2 in respiratory distress.


2008 ◽  
Vol 114 (8) ◽  
pp. 533-541 ◽  
Author(s):  
Lucy Fairclough ◽  
Richard A. Urbanowicz ◽  
Jonathan Corne ◽  
Jonathan R. Lamb

COPD (chronic obstructive pulmonary disease) is a treatable and preventable disease state, characterized by progressive airflow limitation that is not fully reversible. It is a current and growing cause of mortality and morbidity worldwide, with the WHO (World Health Organization) projecting that total deaths attributed to COPD will increase by more than 30% in the next 10 years. The pathological hallmarks of COPD are destruction of the lung parenchyma (pulmonary emphysema), inflammation of the central airways (chronic bronchitis) and inflammation of the peripheral airways (respiratory bronchiolitis). The destructive changes and tissue remodelling observed in COPD are a result of complex interactions between cells of the innate and adaptive immune systems. The focus of the present review is directed towards the role of CD8+ T-lymphocytes, NK (natural killer) cells and NKT cells (NK T-cells). These three classes of killer cell could all play an important part in the pathogenesis of COPD. The observed damage to the pulmonary tissue could be caused in three ways: (i) direct cytotoxic effect against the lung epithelium mediated by the activities of perforin and granzymes, (ii) FasL (Fas ligand)-induced apoptosis and/or (iii) cytokine and chemokine release. The present review considers the role of these killer cells in COPD.


2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Adam Jerzy Białas ◽  
Przemysław Sitarek ◽  
Joanna Miłkowska-Dymanowska ◽  
Wojciech Jerzy Piotrowski ◽  
Paweł Górski

Chronic obstructive pulmonary disease (COPD) is a common preventable and treatable disease, characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. The major risk factor of COPD, which has been proven in many studies, is the exposure to cigarette smoke. However, it is 15–20% of all smokers who develop COPD. This is why we should recognize the pathobiology of COPD as involving a complex interaction between several factors, including genetic vulnerability. Oxidant-antioxidant imbalance is recognized as one of the significant factors in COPD pathogenesis. Numerous exogenous and endogenous sources of ROS are present in pathobiology of COPD. One of endogenous sources of ROS is mitochondria. Although leakage of electrons from electron transport chain and forming of ROS are the effect of physiological functioning of mitochondria, there are various intra- and extracellular factors which may increase this amount and significantly contribute to oxidative-antioxidative imbalance. With the coexistence with impaired antioxidant defence, all these issues lead to oxidative and carbonyl stress. Both of these states play a significant role in pathobiology of COPD and may account for development of major comorbidities of this disease.


2021 ◽  
Author(s):  
Nancy Gomez ◽  
Victoria James ◽  
David Onion ◽  
Lucy Fairclough

Abstract Background: Chronic Obstructive Pulmonary Disease (COPD) is a common inflammatory disease of the airways characterized by irreversible airflow limitation, ranking the third highest cause of death worldwide. Extracellular vesicles (EVs) are important intercellular communication mediators released by cells into their extracellular environment with the capacity to transfer biological signals. EVs involved in COPD hold great potential to understand disease pathogenesis and identify important biomarkers. This systematic review aims to examine all available research on EVs in the pathogenesis and diagnosis of COPD to identify existing knowledge and support further research within the field. Methods: Publications were searched using PubMed and EMBASE with the search terms (Exosomes or extracellular vesicles or microvesicles or microparticles or ectosomes) AND (chronic obstructive pulmonary disease or COPD or emphysema or bronchitis). Results: Initial search yielded 358 papers of which 94 were manually selected for review and 27 were eligible for analyses. The studies were divided into groups according to the role of EVs in pathogenesis, EV origin and cargo, their role in COPD exacerbations and their diagnostic utility. EVs were found to be involved in the mechanism of pathogenesis of COPD, derived from various cell types, as well as containing modified levels of miRNAs. EVs also varied according to the pathophysiological status of disease, therefore presenting a possible method for COPD diagnosis and progress monitoring. Conclusion: The current findings show the limited but good quality research looking at the role of EVs in COPD, demonstrating the need for more studies to better define and provide further insight into the functional characteristics of EV in COPD pathogenesis.


2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Xuewa Guan ◽  
Yanjiao Lu ◽  
Guoqiang Wang ◽  
Peter Gibson ◽  
Fang Chen ◽  
...  

Chronic obstructive pulmonary disease (COPD) is associated with irreversible persistent airflow limitation and enhanced inflammation. The episodes of acute exacerbation (AECOPD) largely depend on the colonized pathogens such as nontypeable Haemophilus influenzae (NTHi), one of the most commonly isolated bacteria. Regulatory T cells (Tregs) are critical in controlling inflammatory immune responses and maintaining tolerance; however, their role in AECOPD is poorly understood. In this study, we hypothesized a regulatory role of Tregs, as NTHi participated in the progress of COPD. Immunological pathogenesis was investigated in a murine COPD model induced by cigarette smoke (CS). NTHi was administrated through intratracheal instillation for an acute exacerbation. Weight loss and lung function decline were observed in smoke-exposed mice. Mice in experimental groups exhibited serious inflammatory responses via histological and cytokine assessment. Expression levels of Tregs and Th17 cells with specific cytokines TGF-β1 and IL-17 were detected to assess the balance of pro-/anti-inflammatory influence partially. Our findings suggested an anti-inflammatory activity of Tregs in CS-induced model. But this activity was suppressed after NTHi administration. Collectively, these data suggested that NTHi might play a necessary role in downregulating Foxp3 to impair the function of Tregs, helping development into AECOPD.


2018 ◽  
Vol 28 (5) ◽  
pp. 613-621 ◽  
Author(s):  
E. V. Bolotova ◽  
V. V. Yavlyanskaya ◽  
A. V. Dudnikova

Cardiorenal relationships in patients with chronic obstructive pulmonary disease (COPD) are discussed in this review. Pathophysiology of cardiorenal syndrome is not fully understood, but supposed to be a complex condition resulted from neurohumoral activation, endothelial dysfunction, proteinuria, oxidative stress, uremia, and other factors. The airflow limitation in COPD could enhance those mechanisms. Recent studies discussed such therapeutic strategies as therapy of haemodymanic or neurohumoral abnormalities, but therapeutic approaches in this disease need further investigations. The lungs could play a role as a part of the cardiorenopulmonary syndrome. Effects of vitamin D on the main parameters of the cardiorenal syndrome and on COPD course have been published. Recent clinical and experimental findings consider vitamin D not only as a marker of the cardiorenal syndrome, but also as a therapeutic target in COPD.


2010 ◽  
Vol 151 (51) ◽  
pp. 2083-2088 ◽  
Author(s):  
Balázs Antus

A kilégzett levegőben mérhető nitrogén-monoxid a legszélesebb körben vizsgált légúti biomarker. A stabil állapotú krónikus obstruktív tüdőbetegségben a kilégzett nitrogén-monoxid-szint hasonló vagy csak kismértékben emelkedett az egészségesekhez képest. Mivel a nitrogén-monoxid-szint szoros összefüggést mutat a légúti eosinophilia mértékével, és mivel az eosinophil típusú légúti gyulladás szteroidokra érzékenyebb, az emelkedett nitrogén-monoxid-szinttel rendelkező betegek jobb válaszkészséget mutatnak az inhalációs vagy szisztémás kortikoszteroidkezelésre. A krónikus obstruktív tüdőbetegség akut exacerbatiója során a kilégzett nitrogén-monoxid szintje megemelkedik, majd ennek kezelése után csökken. Mivel a nitrogén-monoxid-szint és a kezelés során elért légzésfunkciós javulás szoros korrelációt mutat egymással, a nitrogén-monoxid-méréssel a terápiás válasz megjósolható. Összefoglalva: a nitrogén-monoxid-méréssel a krónikus obstruktív tüdőbetegségben szenvedő betegek olyan alcsoportját lehet elkülöníteni, amelynek szteroidérzékenysége nagyobb. Orv. Hetil., 2010, 151, 2083–2088.


2020 ◽  
Vol 28 (3) ◽  
pp. 360-370
Author(s):  
Stanislav N. Kotlyarov ◽  
Anna A. Kotlyarova

Despite all achievements of the modern medicine, the problem of chronic obstructive pulmonary disease (COPD) does not lose its relevance. The current paradigm suggests a key role of macrophages in inflammation in COPD. Macrophages are known to be heterogeneous in their functions. This heterogeneity is determined by their immunometabolic profile and also by peculiarities of lipid homeostasis of cells. Aim. To analyze the role of the ABCA1 transporter, a member of the ABC A subfamily, in the pathogenesis of COPD. The expression of ABCA1 in lung tissues is on the second place after the liver, which shows the important role of the carrier and of lipid homeostasis in the function of lungs. Analysis of the literature shows that participation of the transporter in inflammation consists in regulation of the content of cholesterol in the lipid rafts of the membranes, in phagocytosis and apoptosis. Conclusion. Through regulation of the process of reverse transport of cholesterol in macrophages of lungs, ABCA1 can change their inflammatory response, which makes a significant contribution to the pathogenesis of COPD.


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