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      Clinical Interventions in Aging (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on prevention and treatment of diseases in people over 65 years of age. Sign up for email alerts here.

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      Is Open Access

      Aging and extrapulmonary effects of chronic obstructive pulmonary disease

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          Abstract

          Introduction

          People with COPD have a decline in functional status, but little is known about the rate of decline and factors that contribute. Of particular concern is the decline in cognitive and functional performance. Decrease in cognitive and functional performance will finally lead to decreased health status, sedentary life style and premature frailty.

          Aim

          The aim of this study is to compare functional performance and cognitive status in patients with COPD of different ages and to examine the changes in extrapulmonary effects.

          Patients and methods

          This study included 62 patients with COPD risk class D who were divided into two groups (<70 years, N=30 and >70 years, N=32). Patients first completed the Montreal Cognitive Assessment (MoCA), which is a 30-point test that assesses different cognitive domains, while isometric knee extension (IKE) was measured using a digital handheld dynamometer, and functional exercise level was assessed using the 6-minute walking distance (6MWD) test.

          Results

          The patients’ older age (age higher than 70 years) was associated with a significantly lower body mass index (BMI, 27.50 vs 24.24 kg/m 2; P=0.020), higher vital capacity parameters, forced vital capacity (FVC, 2.74 vs 2.82 L; P=0.799), FVC (%) (73.00 vs 66.50, P=132), forced expiratory volume in the first second (FEV 1, 0.93 vs 1.13 L; P=0.001) and FEV 1 (%) (28.50 vs 30.50, P=0.605). In addition, patients at older age presented a significantly reduced physical activity capacity, 6MWD (385.93 vs 320.84 m, P<0.001) and IKE (24.75 vs 22.55 kgf, P=0.005), as well as higher values for inflammatory biomarkers, C-reactive protein (8.77 vs 3.34 mg/L, P=0.022). Moreover, patients at older age presented significantly lower score at the cognitive assessment, MoCA (23.50 vs 20.00, P<0.001).

          Conclusion

          Elderly COPD patients have reduced exercise capacity and muscle strength, deteriorated cognitive function and increased inflammatory markers. Furthermore, inflammation markers were significantly correlated with muscle strength, walking distance and cognitive impairment.

          Most cited references17

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          The natural history of chronic airflow obstruction.

          A prospective epidemiological study of the early stages of the development of chronic obstructive pulmonary disease was performed on London working men. The findings showed that forced expiratory volume in one second (FEV1) falls gradually over a lifetime, but in most non-smokers and many smokers clinically significant airflow obstruction never develops. In susceptible people, however, smoking causes irreversible obstructive changes. If a susceptible smoker stops smoking he will not recover his lung function, but the average further rates of loss of FEV1 will revert to normal. Therefore, severe or fatal obstructive lung disease could be prevented by screening smokers' lung function in early middle age if those with reduced function could be induced to stop smoking. Infective processes and chronic mucus hypersecretion do not cause chronic airflow obstruction to progress more rapidly. There are thus two largely unrelated disease processes, chronic airflow obstruction and the hypersecretory disorder (including infective processes).
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            Inflammation: gearing the journey to cancer.

            Chronic inflammation plays a multifaceted role in carcinogenesis. Mounting evidence from preclinical and clinical studies suggests that persistent inflammation functions as a driving force in the journey to cancer. The possible mechanisms by which inflammation can contribute to carcinogenesis include induction of genomic instability, alterations in epigenetic events and subsequent inappropriate gene expression, enhanced proliferation of initiated cells, resistance to apoptosis, aggressive tumor neovascularization, invasion through tumor-associated basement membrane and metastasis, etc. Inflammation-induced reactive oxygen and nitrogen species cause damage to important cellular components (e.g., DNA, proteins and lipids), which can directly or indirectly contribute to malignant cell transformation. Overexpression, elevated secretion, or abnormal activation of proinflammatory mediators, such as cytokines, chemokines, cyclooxygenase-2, prostaglandins, inducible nitric oxide synthase, and nitric oxide, and a distinct network of intracellular signaling molecules including upstream kinases and transcription factors facilitate tumor promotion and progression. While inflammation promotes development of cancer, components of the tumor microenvironment, such as tumor cells, stromal cells in surrounding tissue and infiltrated inflammatory/immune cells generate an intratumoral inflammatory state by aberrant expression or activation of some proinflammatory molecules. Many of proinflammatory mediators, especially cytokines, chemokines and prostaglandins, turn on the angiogenic switches mainly controlled by vascular endothelial growth factor, thereby inducing inflammatory angiogenesis and tumor cell-stroma communication. This will end up with tumor angiogenesis, metastasis and invasion. Moreover, cellular microRNAs are emerging as a potential link between inflammation and cancer. The present article highlights the role of various proinflammatory mediators in carcinogenesis and their promise as potential targets for chemoprevention of inflammation-associated carcinogenesis.
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              COPD as a disease of accelerated lung aging.

              There is increasing evidence for a close relationship between aging and chronic inflammatory diseases. COPD is a chronic inflammatory disease of the lungs, which progresses very slowly and the majority of patients are therefore elderly. We here review the evidence that accelerating aging of lung in response to oxidative stress is involved in the pathogenesis and progression of COPD, particularly emphysema. Aging is defined as the progressive decline of homeostasis that occurs after the reproductive phase of life is complete, leading to an increasing risk of disease or death. This results from a failure of organs to repair DNA damage by oxidative stress (nonprogrammed aging) and from telomere shortening as a result of repeated cell division (programmed aging). During aging, pulmonary function progressively deteriorates and pulmonary inflammation increases, accompanied by structural changes, which are described as senile emphysema. Environmental gases, such as cigarette smoke or other pollutants, may accelerate the aging of lung or worsen aging-related events in lung by defective resolution of inflammation, for example, by reducing antiaging molecules, such as histone deacetylases and sirtuins, and this consequently induces accelerated progression of COPD. Recent studies of the signal transduction mechanisms, such as protein acetylation pathways involved in aging, have identified novel antiaging molecules that may provide a new therapeutic approach to COPD.
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                Author and article information

                Journal
                Clin Interv Aging
                Clin Interv Aging
                Clinical Interventions in Aging
                Clinical Interventions in Aging
                Dove Medical Press
                1176-9092
                1178-1998
                2017
                16 August 2017
                : 12
                : 1281-1287
                Affiliations
                [1 ]Department of Pulmonology, University of Medicine and Pharmacy “Victor Babeş”, Timişoara
                [2 ]Faculty of Medicine, Internal Medicine Discipline, Medical Clinical Disciplines I, “Ovidius” University of Constanta, Constanţa
                [3 ]Department of Functional Sciences, “Victor Babes” University of Medicine and Pharmacy, Timişoara
                [4 ]Faculty of Medicine, Pneumophtisiology Department, Medical Clinical Disciplines II, “Ovidius” University Constanta, Constanţa, Romania
                Author notes
                Correspondence: Ariadna Petronela Fildan, Internal Medicine Discipline, Medical Clinical Disciplines I, “Ovidius” University of Constanta, Faculty of Medicine, Aleea Universitatii nr 1, 900470 Constanţa, Romania, Tel +40 741 157 526, Email ariadnapetrofildan@ 123456yahoo.com
                Article
                cia-12-1281
                10.2147/CIA.S145002
                5565244
                28860729
                d953ffb1-c92e-4e2a-94e4-a54e844519b6
                © 2017 Tudorache et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Health & Social care
                aging,inflammation,strength,pulmonary function
                Health & Social care
                aging, inflammation, strength, pulmonary function

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