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      Performance of Multidimensional Severity Scoring Systems in Patients with Post‐Tuberculosis Bronchiectasis

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          Abstract

          Objective

          The aim of this study was to assess the clinical characteristics and outcomes of patients with post‐tuberculosis (post-TB) bronchiectasis. We also evaluated the performance of various multidimensional severity score systems to predict mortality, future exacerbation, and hospitalization.

          Methods

          We conducted a prospective observational cohort study to evaluate the etiology of bronchiectasis in 301 patients. Patients fell into three groups: post-TB (129 [43%]), idiopathic (76 [25%]), and other (96 [32%]) etiologies of bronchiectasis. Four multidimensional grading scales, including the Bronchiectasis Severity Index (BSI), the FACED score, and two derivative versions of the FACED score, Exacerbation (Exa-FACED and E-FACED), were calculated and compared for each patient.

          Results

          Patients with post-TB bronchiectasis were predominantly female (61%) with a mean age of 68±11 years. Moreover, 26% of post-TB bronchiectasis patients were colonized with Pseudomonas aeruginosa. At baseline, patients with post-TB bronchiectasis were older, had higher severity scores, and were more likely to have experienced severe exacerbations that required hospitalization compared to patients with idiopathic bronchiectasis or bronchiectasis arising from other causes. During follow-up, 52% of patients required hospitalization, 58% had frequent (≥2 per year) acute exacerbations, and the overall 5-year mortality rate was 30%. Five-year survival was efficiently predicted by each of the grading scales. Although the modified variations of the FACED outperformed the original FACED scale in predicting forthcoming frequent acute exacerbations and hospitalization, the BSI outperformed all three systems in this regard.

          Conclusion

          Patients with post-TB bronchiectasis had higher severity scores than patients with idiopathic bronchiectasis or bronchiectasis arising from other causes. In addition, all scoring systems performed adequately in 5-year mortality projections. BSI and the modified versions of the FACED outperformed the FACED in predicting forthcoming exacerbations and hospitalizations.

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          Most cited references 9

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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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            Pulmonary tuberculosis, impaired lung function, disability and quality of life in a high-burden setting.

            Tuberculosis treatment clinic in Papua, Indonesia. To document the impact of pulmonary tuberculosis (PTB) on lung function, exercise tolerance and quality of life (QOL). A prospective cohort study of 115 patients with smear-positive PTB followed for 6 months. Demographics, disease history, sputum microbiology, spirometry, 6-minute weight.walk distance (6MWWD) and QOL (modified St George's Respiratory Questionnaire) were measured at diagnosis and at 2 and 6 months. Analysis was restricted to the 69/115 (60%) subjects who attended all follow-up visits. Subjects who attended all visits were less likely than the full cohort to be of Papuan ethnicity (P < 0.05), were more likely to be cured (P < 0.001) and had better lung function at diagnosis (P < 0.05). Significant lung function impairment (forced expiratory volume in 1 second [FEV(1)] <60% predicted) was found in 27/69 (39%) at diagnosis. Although this fell during treatment (P < 0.01), 17/69 (24.6%) had persisting significant lung function impairment at treatment completion. As lung function recovered, exercise tolerance (6MWWD) rose by 12.3% (P < 0.001) and QOL improved (P < 0.001). In a high-burden setting, PTB causes prolonged, significant impairment of lung function, exercise tolerance and QOL. Current measures of disease burden are likely to underestimate the true impact of disease. Earlier diagnosis and disease-modifying treatments may reduce the long-term impact of PTB.
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              Tuberculosis and lung damage: from epidemiology to pathophysiology

              A past history of pulmonary tuberculosis (TB) is a risk factor for long-term respiratory impairment. Post-TB lung dysfunction often goes unrecognised, despite its relatively high prevalence and its association with reduced quality of life. Importantly, specific host and pathogen factors causing lung impairment remain unclear. Host immune responses probably play a dominant role in lung damage, as excessive inflammation and elevated expression of lung matrix-degrading proteases are common during TB. Variability in host genes that modulate these immune responses may determine the severity of lung impairment, but this hypothesis remains largely untested. In this review, we provide an overview of the epidemiological literature on post-TB lung impairment and link it to data on the pathogenesis of lung injury from the perspective of dysregulated immune responses and immunogenetics.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                copd
                copd
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove
                1176-9106
                1178-2005
                14 September 2020
                2020
                : 15
                : 2157-2165
                Affiliations
                [1 ]College of Medicine, King Saud University for Health Sciences , Riyadh, Saudi Arabia
                [2 ]Department of Medicine, Pulmonary Division, Ministry of National Guard-Health Affairs , Riyadh, Saudi Arabia
                [3 ]King Abdullah International Medical Research Center , Riyadh, Saudi Arabia
                [4 ]Department of Medical Imaging, Ministry of National Guard-Health Affairs , Riyadh, Saudi Arabia
                Author notes
                Correspondence: Abdullah AL-Harbi Department of Medicine, Pulmonary Division, Ministry of National Guard-Health Affairs , King Abdulaziz Medical City, PO Box 22490, MC 1443, Riyadh11426, Saudi Arabia Email harbia7@ngha.med.sa
                Article
                261797
                10.2147/COPD.S261797
                7500837
                © 2020 AL-Harbi 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 3, Tables: 6, References: 24, Pages: 9
                Funding
                There is no funding to report.
                Categories
                Original Research

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