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      Transition from Restrictive to Obstructive Lung Function Impairment During Treatment and Follow-Up of Active Tuberculosis

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          Pulmonary tuberculosis (PTB) is associated with many forms of chronic lung disease including the development of chronic airflow obstruction (AFO). However, the nature, evolution and mechanisms responsible for the AFO after PTB are poorly understood. The aim of this study was to examine the progression of changes in lung physiology in patients treated for PTB.


          Immunocompetent, previously healthy, adult patients receiving ambulatory treatment for a first episode of tuberculosis were prospectively followed up with serial lung physiology and quantitative computed tomography (CT) lung scans performed at diagnosis of tuberculosis, 2, 6, 12 and 18 months during and after the completion of treatment.


          Forty-nine patients (median age 26 years; 37.2% males) were included, and 43 were studied. During treatment, lung volumes improved and CT fibrosis scores decreased, but features of AFO and gas trapping emerged, while reduced diffusing capacity (DLco) seen in a majority of patients persisted. Significant increases in total lung capacity (TLC) by plethysmography were seen in the year following treatment completion (median change 5.9% pred., P<0.01) and were driven by large increases in residual volume (RV) (median change +19%pred., P<0.01) but not inspiratory capacity (IC; P=0.41). The change in RV/TLC correlated with significant progression of radiological gas trapping after treatment (P=0.04) but not with emphysema scores. One year after completing treatment, 18.6% of patients had residual restriction (total lung capacity, TLC <80%pred), 16.3% had AFO, 32.6% had gas trapping (RV/TLC>45%), and 78.6% had reduced DLco.


          Simple spirometry alone does not fully reveal the residual respiratory impairments resulting after a first episode of PTB. Changes in physiology evolve after treatment completion, and these findings when taken together, suggest emergence of gas trapping after treatment likely caused by progression of small airway pathology during the healing process.

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          Most cited references 16

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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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            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.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of Chronic Obstructive Pulmonary Disease
                11 May 2020
                : 15
                : 1039-1047
                [1 ]Division of Pulmonology, Department of Medicine, Stellenbosch University , Cape Town, South Africa
                [2 ]University of Cape Town Lung Institute, and Division of Pulmonology, Department of Medicine, University of Cape Town , Cape Town, South Africa
                [3 ]DST/NRF Centre of Excellence for Biomedical Tuberculosis Research; South African Medical Research Council Centre for Tuberculosis Research; Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University , Cape Town, South Africa
                [4 ]Center for Computer Visions and Imaging Biomarkers, Department of Radiology, David Geffen School of Medicine, University of California , Los Angeles, CA, USA
                [5 ]Department of Biostatistics, Fielding School of Public Health, University of California , Los Angeles, CA, USA
                [6 ]Departments of Medicine and Physiology, David Geffen School of Medicine, University of California , Los Angeles, CA, USA
                Author notes
                Correspondence: Brian W Allwood Division of Pulmonology, Department of Medicine, Stellenbosch University , Rm 3013 3rd Floor; Clinical Building; Francie Van Zijl Drive; Medical School, Tygerberg7505, South Africa Email
                © 2020 Allwood 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (

                Page count
                Figures: 4, Tables: 3, References: 20, Pages: 9
                Funding received from the University of Cape Town Lung Institute for funding the radiology component and Global Alliance for TB Drug Development for access to their bio-storage cohort. E.M. is funded by a Strategic Health Innovation Partnership (SHIP) grant from the South African (SA) Department of Science and Technology (DST) and SA Medical Research Council (SAMRC) to the South African Tuberculosis Bioinformatics Initiative (SATBBI), and E.B. received funding from the National Research Foundation (NRF).
                Original Research


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