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      Relationship between obstructive lung disease and non-alcoholic fatty liver disease in the Korean population: Korea National Health and Nutrition Examination Survey, 2007–2010

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          Previous studies have shown that progressive forms of non-alcoholic fatty liver disease (NAFLD) occur frequently in patients with obstructive lung disease (OLD). However, few studies have written about this relationship. This study aimed to investigate the relationship between OLD and NAFLD.

          Subjects and methods

          The Korea National Health and Nutrition Examination Survey is a national population-based, cross-sectional surveillance program that was initiated to assess the health and nutritional status of the Korean population. From 2007 to 2010, 11,738 subjects were enrolled. The subjects were defined as having NAFLD when they had scores higher than −0.640 in a NAFLD liver fat score prediction model, which was a previously validated prediction score. Individuals with forced expiratory volume in one second/forced vital capacity <0.7 were considered to have OLD. The subjects were divided into non-OLD and OLD groups and non-NAFLD and NAFLD groups. All analyses were performed using sample weighting using the complex samples plan.


          The prevalences of NAFLD and OLD were 30.2% and 8.9%, respectively. Although not statistically significant, subjects in the NAFLD group involved a higher tendency of having OLD than did those in the non-NAFLD group (8.5% vs 10.0%, respectively, P=0.060). Subjects with OLD showed a higher tendency to have NAFLD than non-OLD subjects (30.0% vs 33.7%, respectively, P=0.060). NAFLD subjects were at higher odds of OLD (odds ratio=1.334; 95% confidence interval=1.108–1.607, P=0.002) than non-NAFLD subjects, after adjusting for age, sex, and smoking history. OLD subjects were at higher odds of NAFLD (odds ratio=1.556; 95% confidence interval=1.288–1.879, P<0.001) than non-OLD subjects, after adjusting for age, sex, and smoking history.


          This study showed that NAFLD is related to OLD. Clinicians should be aware of possible liver comorbidities in OLD patients and that extrahepatic disease in NAFLD patients may vary more than previously thought.

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          Most cited references 23

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            Differences in interleukin-8 and tumor necrosis factor-alpha in induced sputum from patients with chronic obstructive pulmonary disease or asthma.

            Asthma and chronic obstructive pulmonary disease are characterized by chronic airway inflammation. Studies using bronchoalveolar lavage (BAL) have shown an increased proportion of eosinophils in the BAL fluid from asthmatics compared with that from normal subjects, whereas studies of chronic obstructive pulmonary disease (COPD) have shown increased numbers of neutrophils. Induced sputum allows sampling of respiratory tract secretions from patients and control subjects, providing a noninvasive method of studying airway secretions and allowing characterization of cells and measurement of soluble markers. We investigated whether induced sputum was a useful method of studying airway fluid from patients with moderate to severe COPD and whether it could be used to compare inflammation in this condition with that in asthma. An initial reproducibility study was undertaken. Sputum was induced twice in 13 patients with severe COPD at a 14-d interval. Total and differential cell counts were carried out and were found to be reproducible over this period. Sputum was then induced in 14 patients with COPD, 23 patients with asthma, 12 healthy cigarette smokers, and 16 normal nonsmoking control subjects. We found a significant increase in neutrophils and increased concentrations of tumor necrosis factor-alpha (TNF alpha) and interleukin-8 (IL-8) in the patients with COPD compared with the smoking and nonsmoking control subjects. Interleukin-8, but not TNF alpha, was significantly higher in the COPD group than in the asthmatic group. We conclude that the cytokines TNF alpha and IL-8 may be involved in the inflammation in COPD.
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              Oxidative stress in COPD.

              Oxidative stress is now recognized as a major predisposing factor in the pathogenesis of COPD. Existing therapies for COPD are ineffective at halting disease progression, with bronchodilators being the mainstay of pharmacotherapy, providing symptomatic relief only. It is, therefore, important for a better understanding of the underlying mechanisms by which oxidative stress drives disease pathogenesis to develop novel and more effective therapies. Antioxidant capacity in COPD is substantially reduced as a result of cigarette smoking and exacerbations, with oxidative stress persisting long after the cessation of cigarette smoking or exacerbation, due to the continued production of reactive oxygen species from endogenous sources. We discuss (1) how oxidative stress arises in the lung, (2) how it is neutralized, (3) what genetic factors may predispose to the development of COPD, and (4) how this impacts inflammation and autoimmunity in the development of emphysema and small airways disease. Finally, various strategies have been considered to neutralize the increased oxidative burden present in COPD. This review highlights why current antioxidant strategies have so far failed and what promising alternatives are on the horizon. Moreover, a number of studies have shown that there is no single "magic bullet" to combat oxidative stress, but instead a combination therapy, targeting oxidative stress in the various subcellular compartments, may prove to be more effective in COPD.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                28 August 2018
                : 13
                : 2603-2611
                [1 ]Division of Pulmonary Medicine, Department of Internal Medicine, Institute of Chest Diseases, Severance Hospital, Yonsei University College of Medicine, Seodaemun-gu, Seoul, Korea, tearpoem9@
                [2 ]Center for Preventive Medicine and Public Health, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Korea
                [3 ]Division of Endocrinology, Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seodaemun-gu, Seoul, Korea
                [4 ]Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Korea, tearpoem9@
                Author notes
                Correspondence: Sang Hoon Lee, Division of Pulmonary Medicine, Department of Internal Medicine, Institute of Chest Diseases, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 120-752, Korea, Tel +82 2 2228, 1930 Fax +82 2 393 6884, Email tearpoem9@
                © 2018 Moon et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( 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.

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