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

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 Tuberculos...

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Autores principales: Kim, Tae Hoon, Rhee, Chin Kook, Oh, Yeon-Mok
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Academy of Tuberculosis and Respiratory Diseases 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304328/
https://www.ncbi.nlm.nih.gov/pubmed/30574688
http://dx.doi.org/10.4046/trd.2018.0050
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author Kim, Tae Hoon
Rhee, Chin Kook
Oh, Yeon-Mok
author_facet Kim, Tae Hoon
Rhee, Chin Kook
Oh, Yeon-Mok
author_sort Kim, Tae Hoon
collection PubMed
description 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 healthrelated 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.
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spelling pubmed-63043282019-01-01 Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation Kim, Tae Hoon Rhee, Chin Kook Oh, Yeon-Mok Tuberc Respir Dis (Seoul) Original Article 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 healthrelated 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. The Korean Academy of Tuberculosis and Respiratory Diseases 2019-01 2018-12-19 /pmc/articles/PMC6304328/ /pubmed/30574688 http://dx.doi.org/10.4046/trd.2018.0050 Text en Copyright©2019. The Korean Academy of Tuberculosis and Respiratory Diseases http://creativecommons.org/licenses/by-nc/4.0/ It is identical to the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/)
spellingShingle Original Article
Kim, Tae Hoon
Rhee, Chin Kook
Oh, Yeon-Mok
Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation
title Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation
title_full Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation
title_fullStr Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation
title_full_unstemmed Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation
title_short Factors Associated with Indacaterol Response in Tuberculosis-Destroyed Lung with Airflow Limitation
title_sort factors associated with indacaterol response in tuberculosis-destroyed lung with airflow limitation
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304328/
https://www.ncbi.nlm.nih.gov/pubmed/30574688
http://dx.doi.org/10.4046/trd.2018.0050
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