Poor adherence to chronic obstructive pulmonary disease medications in primary care: Role of age, disease burden and polypharmacy

2017 ◽  
Vol 17 (12) ◽  
pp. 2500-2506 ◽  
Author(s):  
Davide L. Vetrano ◽  
Elisa Bianchini ◽  
Graziano Onder ◽  
Iacopo Cricelli ◽  
Claudio Cricelli ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Primary Care ◽  
Pulmonary Disease ◽  
Disease Burden ◽  
Poor Adherence ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Role of exhaled nitric oxide in predicting steroid response in chronic obstructive pulmonary disease

2010 ◽  
Vol 151 (51) ◽  
pp. 2083-2088 ◽  
Author(s):  
Balázs Antus
Keyword(s):  
Nitric Oxide ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Exhaled Nitric Oxide ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Steroid Response

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.

Participation of ABCA1 transporter in development of chronic obstructive pulmonary disease

2020 ◽  
Vol 28 (3) ◽  
pp. 360-370
Author(s):  
Stanislav N. Kotlyarov ◽  
Anna A. Kotlyarova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Significant Contribution ◽  
Modern Medicine ◽  
Lipid Homeostasis ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Reverse Transport ◽  
Current Paradigm

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.

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.

scholarly journals Nutrition in chronic obstructive pulmonary disease: A review

2015 ◽  
Vol 3 (4) ◽  
pp. 151-154 ◽  
Author(s):  
Gautam Rawal ◽  
Sankalp Yadav
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Exercise Tolerance ◽  
Muscle Wasting ◽  
Nutritional Supplement ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Supplement Therapy

AbstractCachexia and muscle wasting is a frequent but partly reversible complication in patients with chronic obstructive pulmonary disease (COPD), and affects the disease progression and prognosis. Weight loss in COPD is a consequence of increased energy requirements unbalanced by dietary intake. Nutritional supplement therapy has been shown to be effective for maintaining and improving the muscle strength and exercise tolerance in poorly nourished COPD patients, thereby decreasing morbidity and mortality. This mini review discusses the role of nutritional supplement therapy in the treatment of COPD.

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