Browse > Article
http://dx.doi.org/10.4046/trd.2018.0050

Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation  

Kim, Tae Hoon (Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine)
Rhee, Chin Kook (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)
Oh, Yeon-Mok (Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine)
Publication Information
Tuberculosis and Respiratory Diseases / v.82, no.1, 2019 , pp. 35-41 More about this Journal
Abstract
Background: Pulmonary tuberculosis can result in anatomical sequelae, and cause airflow limitation. However, there are no treatment guidelines for patients with a tuberculosis-destroyed lung. Recently, indacaterol effectiveness in chronic obstructive pulmonary disease (COPD) patients with Tuberculosis history (INFINITY) study revealed indacaterol provided bronchodilation and symptom improvement in COPD patients with a tuberculosis-destroyed lung. Methods: We conducted a post-hoc subgroup analysis of the randomized controlled trial, the INFINITY study, to determine factors associated with indacaterol response in a tuberculosis-destroyed lung with airflow limitation. Data from 68 patients treated with inhaled indacaterol, were extracted and analyzed. Factors associated with the response of forced expiratory volume in one second ($FEV_1$) to indacaterol treatment, were determined using linear regression analysis. Results: Of 62 patients included, 68% were male, and 52% had history of cigarette smoking. Patients revealed mean $FEV_1$ of 50.5% of predicted value with mean improvement of 81.3 mL in $FEV_1$ after indacaterol treatment for 8 weeks. Linear regression analysis revealed factors associated with response of $FEV_1$ to indacaterol included a short duration of smoking history, and high short-acting bronchodilator response. When patients with history of smoking were excluded, factors associated with response of $FEV_1$ to indacaterol included high short-acting bronchodilator response, and poor health-related quality of life score as measured by St. George's Respiratory Questionnaire for COPD. Conclusion: In a tuberculosis-destroyed lung with airflow limitation, short-acting bronchodilator response and smoking history can play a critical role in predicting outcomes of indacaterol treatment.
Keywords
Tuberculosis; Pulmonary Disease, Chronic Obstructive; Indacaterol; Smoking;
Citations & Related Records
Times Cited By KSCI : 1  (Citation Analysis)
연도 인용수 순위
1 Kohansal R, Martinez-Camblor P, Agusti A, Buist AS, Mannino DM, Soriano JB. The natural history of chronic airflow obstruction revisited: an analysis of the Framingham offspring cohort. Am J Respir Crit Care Med 2009;180:3-10.   DOI
2 Ji W, Lim MN, Bak SH, Hong SH, Han SS, Lee SJ, et al. Differences in chronic obstructive pulmonary disease phenotypes between non-smokers and smokers. Clin Respir J 2018;12:666-73.   DOI
3 Lamprecht B, McBurnie MA, Vollmer WM, Gudmundsson G, Welte T, Nizankowska-Mogilnicka E, et al. COPD in never smokers: results from the population-based burden of obstructive lung disease study. Chest 2011;139:752-63.   DOI
4 Zhou Y, Wang C, Yao W, Chen P, Kang J, Huang S, et al. COPD in Chinese nonsmokers. Eur Respir J 2009;33:509-18.   DOI
5 Ramirez-Venegas A, Sansores RH, Perez-Padilla R, Regalado J, Velazquez A, Sanchez C, et al. Survival of patients with chronic obstructive pulmonary disease due to biomass smoke and tobacco. Am J Respir Crit Care Med 2006;173:393-7.   DOI
6 Rezende Goncalves J, Corso Pereira M, Figueiras Pedreira De Cerqueira EM, Oliveira Magro D, Mello Moreira M, Paschoal IA. Severe obstructive disease: similarities and differences between smoker and non-smoker patients with COPD and/or bronchiectasis. Rev Port Pneumol 2013;19:13-8.   DOI
7 Leung CC, Yew WW, Chan CK, Tam CM, Lam CW, Chang KC, et al. Smoking and tuberculosis in Hong Kong. Int J Tuberc Lung Dis 2003;7:980-6.
8 Zhang J, Lin XF, Bai CX. Comparison of clinical features between non-smokers with COPD and smokers with COPD: a retrospective observational study. Int J Chron Obstruct Pulmon Dis 2014;9:57-63.   DOI
9 Camp PG, Ramirez-Venegas A, Sansores RH, Alva LF, Mc-Dougall JE, Sin DD, et al. COPD phenotypes in biomass smoke- versus tobacco smoke-exposed Mexican women. Eur Respir J 2014;43:725-34.   DOI
10 Kim HY, Song KS, Goo JM, Lee JS, Lee KS, Lim TH. Thoracic sequelae and complications of tuberculosis. Radiographics 2001;21:839-58.   DOI
11 Menezes AM, Hallal PC, Perez-Padilla R, Jardim JR, Muino A, Lopez MV, et al. Tuberculosis and airflow obstruction: evidence from the PLATINO study in Latin America. Eur Respir J 2007;30:1180-5.   DOI
12 World Health Organization Global tuberculosis report, 2017 [Internet]. Geneva: World Health Organization; 2017 [cited 2018 Apr 1]. Available from: http://appswhoint/iris/bitstream/handle/10665/259366/9789241565516-engpdf?sequence=1.
13 Harries AD, Ade S, Burney P, Hoa NB, Schluger NW, Castro JL. Successfully treated but not fit for purpose: paying attention to chronic lung impairment after TB treatment. Int J Tuberc Lung Dis 2016;20:1010-4.   DOI
14 Jung JW, Choi JC, Shin JW, Kim JY, Choi BW, Park IW. Pulmonary impairment in tuberculosis survivors: the Korean National Health and Nutrition Examination Survey 2008-2012. PLoS One 2015;10:e0141230.   DOI
15 Pasipanodya JG, Miller TL, Vecino M, Munguia G, Garmon R, Bae S, et al. Pulmonary impairment after tuberculosis. Chest 2007;131:1817-24.   DOI
16 Byrne AL, Marais BJ, Mitnick CD, Lecca L, Marks GB. Tuberculosis and chronic respiratory disease: a systematic review. Int J Infect Dis 2015;32:138-46.   DOI
17 Yum HK, Park IN. Effect of inhaled tiotropium on spirometric parameters in patients with tuberculous destroyed lung. Tuberc Respir Dis 2014;77:167-71.   DOI
18 Hanania NA, Celli BR, Donohue JF, Martin UJ. Bronchodilator reversibility in COPD. Chest 2011;140:1055-63.   DOI
19 Kim CJ, Yoon HK, Park MJ, Yoo KH, Jung KS, Park JW, et al. Inhaled indacaterol for the treatment of COPD patients with destroyed lung by tuberculosis and moderate-to-severe airflow limitation: results from the randomized INFINITY study. Int J Chron Obstruct Pulmon Dis 2017;12:1589-96.   DOI
20 Chakrabarti B, Calverley PM, Davies PD. Tuberculosis and its incidence, special nature, and relationship with chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis 2007;2:263-72.
21 Bleecker ER, Emmett A, Crater G, Knobil K, Kalberg C. Lung function and symptom improvement with fluticasone propionate/salmeterol and ipratropium bromide/albuterol in COPD: response by beta-agonist reversibility. Pulm Pharmacol Ther 2008;21:682-8.   DOI
22 Tashkin D, Kesten S. Long-term treatment benefits with tiotropium in COPD patients with and without short-term bronchodilator responses. Chest 2003;123:1441-9.   DOI
23 Hanania NA, Sharafkhaneh A, Celli B, Decramer M, Lystig T, Kesten S, et al. Acute bronchodilator responsiveness and health outcomes in COPD patients in the UPLIFT trial. Respir Res 2011;12:6.   DOI
24 Forey BA, Thornton AJ, Lee PN. Systematic review with metaanalysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema. BMC Pulm Med 2011;11:36.   DOI
25 Burgel PR, Le Gros V, Decuypere L, Bourdeix I, Perez T, Deslee G. Immediate salbutamol responsiveness does not predict long-term benefits of indacaterol in patients with chronic obstructive pulmonary disease. BMC Pulm Med 2017;17:25.   DOI
26 Rhee CK, Yoo KH, Lee JH, Park MJ, Kim WJ, Park YB, et al. Clinical characteristics of patients with tuberculosis-destroyed lung. Int J Tuberc Lung Dis 2013;17:67-75.   DOI