scholarly journals Chronic Obstructive Pulmonary Disease: Epidemiology, Biomarkers, and Paving the Way to Lung Cancer

2021 ◽  
Vol 10 (13) ◽  
pp. 2889
Author(s):  
Klára Szalontai ◽  
Nikolett Gémes ◽  
József Furák ◽  
Tünde Varga ◽  
Patrícia Á. Neuperger ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Alveolar Wall ◽  
Obstructive Pulmonary Disease ◽  
Major Health Problem ◽  
Chronic Inflammatory Response ◽  
Disease Epidemiology

Chronic obstructive pulmonary disease (COPD), the frequently fatal pathology of the respiratory tract, accounts for half a billion cases globally. COPD manifests via chronic inflammatory response to irritants, frequently to tobacco smoke. The progression of COPD from early onset to advanced disease leads to the loss of the alveolar wall, pulmonary hypertension, and fibrosis of the respiratory epithelium. Here, we focus on the epidemiology, progression, and biomarkers of COPD with a particular connection to lung cancer. Dissecting the cellular and molecular players in the progression of the disease, we aim to shed light on the role of smoking, which is responsible for the disease, or at least for the more severe symptoms and worse patient outcomes. We summarize the inflammatory conditions, as well as the role of EMT and fibroblasts in establishing a cancer-prone microenvironment, i.e., the soil for ‘COPD-derived’ lung cancer. We highlight that the major health problem of COPD can be alleviated via smoking cessation, early diagnosis, and abandonment of the usage of biomass fuels on a global basis.

Role of Capnograghy during weaning from mechanical ventilation in patients with chronic obstructive pulmonary disease

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Ramy Karem Ali Ali ◽  
Yasser Mosafa Mohammed Mostafa ◽  
Tamer Mohammed Ali
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mechanical Ventilation ◽  
Pulmonary Disease ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Weaning From Mechanical Ventilation ◽  
Cross Sectional ◽  
Obstructive Pulmonary Disease ◽  
Chronic Inflammatory Response

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.

scholarly journals Chronic Obstructive Pulmonary Disease (COPD) and Its Association with Lung Cancer: Molecular Mechanism and Therapeutic Targets

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Shanmugam G ◽  
◽  
Rakshit S ◽  
Sarkar K ◽  
◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Therapeutic Targets ◽  
Epidemiological Studies ◽  
Chronic Obstructive ◽  
Lung Carcinogenesis ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients

Chronic Obstructive Pulmonary Disease (COPD) and Lung cancer are the major reasons for lung disease-related mortality worldwide. Chronic inflammation is a key attribute of COPD and a potential driver of lung carcinogenesis. Among various environmental risk factors, cigarette smoke plays a crucial role in the development and progression of COPD and lung cancer. Several epidemiological studies show that COPD patients are at a greater risk of developing lung cancer independently of cigarette smoking which suggests the role of genetic predisposition in the disease development. Uncovering the mechanistic link between these two diseases is hampered due to their heterogeneous nature: each is characterized by several sub-phenotypes of diseases. This review focuses on the nature of the link between the two diseases and specific mechanisms that occur in both COPD and lung cancer, some of the therapeutic targets which are currently employed, and the role of gene-editing technology to combat these debilitating lung-inflammatory disorders.

scholarly journals The Role of Mitochondria and Oxidative/Antioxidative Imbalance in Pathobiology of Chronic Obstructive Pulmonary Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Adam Jerzy Białas ◽  
Przemysław Sitarek ◽  
Joanna Miłkowska-Dymanowska ◽  
Wojciech Jerzy Piotrowski ◽  
Paweł Górski
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Airflow Limitation ◽  
Carbonyl Stress ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Chronic Inflammatory Response ◽  
Transport Chain ◽  
Significant Factors

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.

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