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      Effects of inhaler therapy on mortality in patients with tuberculous destroyed lung and airflow limitation

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          Although patients with tuberculous destroyed lung (TDL) receive long-acting muscarinic antagonist (LAMA) inhaler therapy, its effectiveness is not clear. This study evaluated the effect of LAMA inhaler therapy on mortality in patients with TDL and airflow limitation.

          Patients and methods

          A retrospective cohort of 683 patients with TDL and airflow limitation was analyzed in this study. The mortality was compared between 177 patients treated with LAMA inhalers >360 days (LAMA group) and 506 patients not treated with LAMA inhalers or treated with LAMA inhalers for <360 days (non-LAMA group). Risk factors for mortality were analyzed with Cox proportional hazards models and survival analysis was performed after propensity score matching.


          Patients in the LAMA group appeared to have worse baseline characteristics, older mean age, lower lung function, higher X-ray severity, and were more likely to receive long-term oxygen therapy than those in the non-LAMA group. On multivariate analysis, LAMA inhaler usage was independently associated with lower risk of mortality (HR, 0.405; P=0.006) after adjusting age, gender, body mass index, smoking history, Charlson Comorbidity Index, lung function, X-ray severity, and long-term oxygen therapy. After propensity score matching to adjust for the above unbalanced baseline characteristics, patients in the LAMA group tended to have a better prognosis than those in the non-LAMA group (121 patients in each group, 5-year mortality rate: 2.5% vs 9.1%, P=0.057). If we performed the same analysis of propensity score matching even after excluding patients with corticosteroids/long-acting beta-2 agonist (ICS/LABA) usage, patients in the LAMA group had a better prognosis than those in the non-LAMA group (64 patients in each group, 5-year mortality rate: 3.1% vs 14.1%, P=0.039).


          LAMA inhaler treatment might reduce mortality in patients with TDL and airflow limitation.

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          Most cited references 21

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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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            Prior TB, smoking, and airflow obstruction: a cross-sectional analysis of the Guangzhou Biobank Cohort Study.

            Prior pulmonary TB has been shown to be associated with a higher risk of airflow obstruction, which is the hallmark of COPD, but whether smoking modifies this relationship is unclear. We investigated the relationships between prior TB, smoking, and airflow obstruction in a Chinese population sample. Participants in the Guangzhou Biobank Cohort Study underwent spirometry, chest radiography, and a structured interview on lifestyle and exposures. Prior TB was defined as the presence of radiologic evidence suggestive of inactive TB. Airflow obstruction was based on spirometric criteria. The prevalence of prior TB in this sample (N = 8,066, mean age: 61.9 years) was 24.2%. After controlling for sex, age, and smoking exposure, prior TB remained independently associated with an increased risk of airflow obstruction (odds ratio = 1.37; 95% CI, 1.13-1.67). Further adjustment for exposure to passive smoking, biomass fuel, and dust did not alter the relationship. Smoking did not modify the relationship between prior TB and airflow obstruction. Prior TB is an independent risk factor for airflow obstruction, which may partly explain the higher prevalence of COPD in China. Clinicians should be aware of this long-term risk in individuals with prior TB, irrespective of smoking status, particularly in patients from countries with a high TB burden.
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              Chronic obstructive airways disease following treated pulmonary tuberculosis.

              Seventy-one subjects who had previously been treated for tuberculosis up to 16 years before underwent pulmonary function assessment. Evidence of airways obstruction was found in 48 (68%). There was an inverse relationship between the extent of the disease on the original chest radiograph and the forced expired volume in one second (FEV1). A similar inverse relationship between the amount of sputum produced and the FEV1 and the original chest radiograph was also found. Treated pulmonary tuberculosis is a cause of significant chronic obstructive airways disease.

                Author and article information

                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                05 March 2019
                : 15
                : 377-387
                [1 ]Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea, ymoh55@ 123456amc.seoul.kr
                [2 ]Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, Korea
                [3 ]Division of Pulmonary, Allergy and Critical Care Medicine, Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea
                [4 ]Department of Clinical Epidemiology and Biostatistics, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea
                Author notes
                Correspondence: Yeon-Mok Oh, Department of Pulmonary and Critical Care Medicine, Asan Medical Center University of Ulsan College of Medicine, 88, Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, South Korea, Tel +82 23 010 3136, Fax +82 23 010 6968, Email ymoh55@ 123456amc.seoul.kr

                These authors contributed equally to this work

                © 2019 Kim 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.

                Original Research


                tuberculosis, long-acting muscarinic antagonist, propensity score, survival


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