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      Emphysema and bronchiectasis in COPD patients with previous pulmonary tuberculosis: computed tomography features and clinical implications

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          Abstract

          Background

          Pulmonary tuberculosis (PTB) is a risk factor for COPD, but the clinical characteristics and the chest imaging features (emphysema and bronchiectasis) of COPD with previous PTB have not been studied well.

          Methods

          The presence, distribution, and severity of emphysema and bronchiectasis in COPD patients with and without previous PTB were evaluated by high-resolution computed tomography (HRCT) and compared. Demographic data, respiratory symptoms, lung function, and sputum culture of Pseudomonas aeruginosa were also compared between patients with and without previous PTB.

          Results

          A total of 231 COPD patients (82.2% ex- or current smokers, 67.5% male) were consecutively enrolled. Patients with previous PTB (45.0%) had more severe ( p=0.045) and longer history ( p=0.008) of dyspnea, more exacerbations in the previous year ( p=0.011), and more positive culture of P. aeruginosa ( p=0.001), compared with those without PTB. Patients with previous PTB showed a higher prevalence of bronchiectasis ( p<0.001), which was more significant in lungs with tuberculosis (TB) lesions, and a higher percentage of more severe bronchiectasis (Bhalla score ≥2, p=0.031), compared with those without previous PTB. The overall prevalence of emphysema was not different between patients with and without previous PTB, but in those with previous PTB, a higher number of subjects with middle ( p=0.001) and lower ( p=0.019) lobe emphysema, higher severity score ( p=0.028), higher prevalence of panlobular emphysema ( p=0.013), and more extensive centrilobular emphysema ( p=0.039) were observed. Notably, in patients with TB lesions localized in a single lung, no difference was found in the occurrence and severity of emphysema between the 2 lungs.

          Conclusion

          COPD patients with previous PTB had unique features of bronchiectasis and emphysema on HRCT, which were associated with significant dyspnea and higher frequency of severe exacerbations. While PTB may have a local effect on bronchiectasis, its involvement in airspace damage in COPD may be extensive, probably through interactions with cigarette smoke.

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          Most cited references 31

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          Prevalence of COPD in five Colombian cities situated at low, medium, and high altitude (PREPOCOL study).

          The prevalence of COPD in Colombia is unknown. This study aimed to investigate COPD prevalence in five Colombian cities and measure the association between COPD and altitude. A cross-sectional design and a random, multistage, cluster-sampling strategy were used to provide representative samples of adults aged >or= 40 years. Each participant was interviewed (validated Spanish version of the Ferris Respiratory Questionnaire) and performed spirometry before and after 200 microg of inhaled salbutamol, using a portable spirometer according to American Thoracic Society recommendations. COPD definitions were as follows: (1) spirometric: fixed ratio (primary definition): FEV1/FVC or= 3 months every year during >or= 2 consecutive years (chronic bronchitis). Analysis was performed using statistical software. A total of 5,539 orsubjects were included. The overall COPD prevalence using the primary definition (spirometric) was 8.9%, ranging from 6.2% in Barranquilla to 13.5% in Medellín. The prevalence measured by the spirometric definition was higher than medical (2.8%) and clinical (3.2%) definitions. After the logistic regression analysis, the factors related with COPD were age >or= 60 years, male gender, history of tuberculosis, smoking, wood smoke exposure >or= 10 years, and very low education level. There was a nonsignificant tendency toward larger prevalence with higher altitude. COPD is an important health burden in Colombia. Additional studies are needed to establish the real influence of altitude on COPD prevalence.
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            Chronic pulmonary function impairment caused by initial and recurrent pulmonary tuberculosis following treatment.

            A study was undertaken to establish the chronic effect of initial and recurrent treated pulmonary tuberculosis on impairment of lung function. A total of 27 660 black South African gold miners who had reliable pulmonary function tests from January 1995 to August 1996 were retrospectively followed for the incidence of pulmonary tuberculosis to 1970. The lung function measurements in 1995-6 were related to the number of previous episodes of tuberculosis and to the time that had lapsed from the diagnosis of the last episode of tuberculosis to the lung function test. Miners without tuberculosis or pneumoconiosis served as a comparison group. There were 2137 miners who had one episode of tuberculosis, 366 who had two, and 96 who had three or more episodes. The average time between the diagnosis of the last episode of tuberculosis and the lung function test was 4.6 years (range one month to 31 years). The loss of lung function was highest within six months of the diagnosis of tuberculosis and stabilised after 12 months when the loss was considered to be chronic. The estimated average chronic deficit in forced expiratory volume in one second (FEV(1)) after one, two, and three or more episodes of tuberculosis was 153 ml, 326 ml, and 410 ml, respectively. The corresponding deficits for forced vital capacity (FVC) were 96 ml, 286 ml, and 345 ml. The loss of function due to tuberculosis was not biased by the presence of HIV as HIV positive and HIV negative subjects had similar losses. The percentage of subjects with chronic airflow impairment (FEV(1) <80% predicted) was 18.4% in those with one episode, 27.1% in those with two, and 35.2% in those with three or more episodes of tuberculosis. Tuberculosis can cause chronic impairment of lung function which increases incrementally with the number of episodes of tuberculosis. Clearly, prevention of tuberculosis and its effect on lung function is important and can be achieved by early detection and by reduction of the risk of tuberculosis through intervention on risk factors such as HIV, silica dust exposure, silicosis, and socioeconomic factors.
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              Pulmonary impairment after tuberculosis.

              Pulmonary impairment subsequent to a cure of pulmonary tuberculosis has been described only in selected populations. We compared pulmonary function in a case-control study of 107 prospectively identified patients with pulmonary tuberculosis who had completed at least 20 weeks of therapy and 210 patients with latent tuberculosis infection (LTBI). Both groups had similar risk factors for pulmonary impairment. Impairment was present in 59% of tuberculosis subjects and 20% of LTBI control subjects. FVC, FEV1, FEV1/FVC ratio, and the midexpiratory phase of forced expiratory flow were significantly lower in the treated pulmonary tuberculosis patients than in the comparison group. Ten patients with a history of pulmonary tuberculosis (9.4%) had less than half of their expected vital capacity vs one patient (0.53%) in the LTBI group. Another 42 patients (39%) with tuberculosis had between 20% and 50% of the expected vital capacity vs 36 patients with LTBI (17%). After adjusting for risk, survivors of tuberculosis were 5.4 times more likely to have abnormal pulmonary function test results than were LTBI patients (p > 0.001; 95% confidence interval, 2.98 to 9.68). Birth in the United States (odds ratio [OR], 2.64; p = 0.003) and age (OR, 1.03; p = 0.005) increased the odds of impairment. Pulmonary impairment was more common in cigarette smokers; however, after adjusting for demographic and other risk factors, the difference did not reach statistical significance (p = 0.074). These findings indicate that pulmonary impairment after tuberculosis is associated with disability worldwide and support more aggressive case prevention strategies and posttreatment evaluation. For many persons with tuberculosis, a microbiological cure is the beginning not the end of their illness.
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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
                24 January 2018
                : 13
                : 375-384
                Affiliations
                [1 ]Department of Respiratory and Critical Care Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing
                [2 ]Department of Radiology, Beijing Tongren Hospital, Capital Medical University, Beijing
                [3 ]Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing, China
                Author notes
                Correspondence: Yongchang Sun, Department of Respiratory and Critical Care Medicine, Beijing Tongren Hospital, Capital Medical University, 1 Dong Jiao Min Xiang, Dongcheng District, Beijing 100730, China, Tel +86 156 1196 3697, Email suny@ 123456bjmu.edu.cn
                Article
                copd-13-375
                10.2147/COPD.S152447
                5788930
                © 2018 Jin 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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                Original Research

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