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      Quantitative computed tomography features and clinical manifestations associated with the extent of bronchiectasis in patients with moderate-to-severe COPD

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          Abstract

          Background

          Few studies have investigated the quantitative computed tomography (CT) features associated with the severity of bronchiectasis in COPD patients. The purpose of this study was to identify the quantitative CT features and clinical values to determine the extent of bronchiectasis in moderate-to-severe COPD patients.

          Methods

          A total of 127 moderate-to-severe COPD patients were selected from the cohort of COPD in Dusty Areas (CODA). The study subjects were classified into three groups according to the extent of bronchiectasis on CT: no bronchiectasis, mild bronchiectasis, and moderate-to-severe bronchiectasis. The three groups were compared with respect to demographic data, symptoms, medical history, serum inflammatory markers, pulmonary function, and quantitative CT values.

          Results

          Among 127 moderate-to-severe COPD subjects, 73 patients (57.5%) were detected to have bronchiectasis, 51 patients (40.2%) to have mild bronchiectasis, and 22 patients (17.3%) to have moderate-to-severe bronchiectasis. Compared with COPD patients without bronchiectasis, those with bronchiectasis were older and had higher frequency of prior tuberculosis, lower prevalence of bronchodilator reversibility (BDR), and more severe air trapping ( P < 0.05). Moderate-to-severe bronchiectasis patients had lower body mass index (BMI), higher frequency of prior tuberculosis, lower prevalence of BDR, worse pulmonary function, and more severe air trapping ( P < 0.05) than those in the mild bronchiectasis group.

          Conclusion

          Moderate-to-severe bronchiectasis was associated with a history of pulmonary tuberculosis, lower BMI, severe airflow obstruction, and lower BDR in moderate-to-severe COPD patients. Quantitative analysis of CT showed that severe air trapping was associated with the extent of bronchiectasis in these patients.

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          Most cited references 21

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          Quantitative assessment of emphysema, air trapping, and airway thickening on computed tomography.

          The severity of chronic obstructive pulmonary disease (COPD) is evaluated not only by airflow limitation but also by factors such as exercise capacity and body mass index. Recent advances in CT technology suggest that it might be a useful tool for evaluating the severity of the disease components of COPD. The aim of this study is to evaluate the correlation between the parameters measured on volumetric CT, including the extent of emphysema, air trapping, and airway thickening, and clinical parameters. CT scans were performed in 34 patients with COPD at full inspiration and expiration. We used in-house software to measure CT parameters, including volume fraction of emphysema (V(950)), mean lung density (MLD), CT air trapping index (CT ATI), segmental bronchial wall area (WA), lumen area (LA), and wall area percent (WA%). We found that the CT parameters were correlated with the pulmonary function test (PFT) results, body mass index (BMI), the modified Medical Research Council Dyspnea scale (MMRC scale), the six-minute-walk distance (6MWD), and the BODE index. V(950 insp) correlated to the BMI, FEV(1), 6MWD, and the BODE index. The CT ATI correlated with the physiologic ATI (VC-FVC) (R=0.345, p=0.045) and the MMRC scale (R=0.532, p=0.001). There was a positive correlation between the WA% and the BMI (R=0.563, p<0.001). MLD(exp) showed the strongest correlation with the BODE index (R= -0.756, p<0.001). We conclude that the severity of emphysema and air trapping measured on CT correlated with the PFT parameters 6MWD and BMI.
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            Thoracic sequelae and complications of tuberculosis.

             H. Kim,  K Song,  J Goo (2015)
            Pulmonary tuberculosis is caused by Mycobacterium tuberculosis when droplet nuclei laden with bacilli are inhaled. In accordance with the virulence of the organism and the defenses of the host, tuberculosis can occur in the lungs and in extrapulmonary organs. A variety of sequelae and complications can occur in the pulmonary and extrapulmonary portions of the thorax in treated or untreated patients. These can be categorized as follows: (a) parenchymal lesions, which include tuberculoma, thin-walled cavity, cicatrization, end-stage lung destruction, aspergilloma, and bronchogenic carcinoma; (b) airway lesions, which include bronchiectasis, tracheobronchial stenosis, and broncholithiasis; (c) vascular lesions, which include pulmonary or bronchial arteritis and thrombosis, bronchial artery dilatation, and Rasmussen aneurysm; (d) mediastinal lesions, which include lymph node calcification and extranodal extension, esophagomediastinal or esophagobronchial fistula, constrictive pericarditis, and fibrosing mediastinitis; (e) pleural lesions, which include chronic empyema, fibrothorax, bronchopleural fistula, and pneumothorax; and (f) chest wall lesions, which include rib tuberculosis, tuberculous spondylitis, and malignancy associated with chronic empyema. These varieties of radiologic manifestations can mimic other disease entities. Therefore, recognition and understanding of the radiologic manifestations of the thoracic sequelae and complications of tuberculosis are important to facilitate diagnosis.
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              The pathophysiology of bronchiectasis

               Paul King (2009)
              Bronchiectasis is defined by permanent and abnormal widening of the bronchi. This process occurs in the context of chronic airway infection and inflammation. It is usually diagnosed using computed tomography scanning to visualize the larger bronchi. Bronchiectasis is also characterized by mild to moderate airflow obstruction. This review will describe the pathophysiology of noncystic fibrosis bronchiectasis. Studies have demonstrated that the small airways in bronchiectasis are obstructed from an inflammatory infiltrate in the wall. As most of the bronchial tree is composed of small airways, the net effect is obstruction. The bronchial wall is typically thickened by an inflammatory infiltrate of lymphocytes and macrophages which may form lymphoid follicles. It has recently been demonstrated that patients with bronchiectasis have a progressive decline in lung function. There are a large number of etiologic risk factors associated with bronchiectasis. As there is generally a long-term retrospective history, it may be difficult to determine the exact role of such factors in the pathogenesis. Extremes of age and smoking/chronic obstructive pulmonary disease may be important considerations. There are a variety of different pathogens involved in bronchiectasis, but a common finding despite the presence of purulent sputum is failure to identify any pathogenic microorganisms. The bacterial flora appears to change with progression of disease.
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                Author and article information

                Journal
                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
                1176-9106
                1178-2005
                2018
                01 May 2018
                : 13
                : 1421-1431
                Affiliations
                [1 ]Department of Radiology, School of Medicine, Kangwon National University, Chuncheon, Repubilc of Korea
                [2 ]Department of Radiology, Kangwon National University Hospital, Chuncheon, Republic of Korea
                [3 ]Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon, Republic of Korea
                [4 ]Department of Internal Medicine and Environmental Health Center, Kangwon National University Hospital, Chuncheon, Republic of Korea
                [5 ]Data Analysis Center, Kangwon National University, Chuncheon, Republic of Korea
                Author notes
                Correspondence: Woo Jin Kim, Department of Internal Medicine, School of Medicine, Kangwon National University, 1 Kangwondaehak-gil, Chuncheon, Gangwon-do, 24341, Republic of Korea, Tel +82 32 258 9364, Fax +82 32 258 2404, Email wjkim47@ 123456gmail.com
                Article
                copd-13-1421
                10.2147/COPD.S157953
                5936002
                © 2018 Bak 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.

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