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

Background

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.

Methods

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.

Results

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.

Conclusion

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.

Informations de copyright

© 2020 Allwood et al.

Déclaration de conflit d'intérêts

Dr Brian Allwood reports speaker honoraria from Novartis, outside the submitted work. Professor Kim reports personal fee from MedQIA outside the submitted work. Professor Richard van Zyl-Smit reports personal fees from AstraZeneca CIPLA, Roche, Novartis, Pfizer, ASPEN/GSK and MSD outside the submitted work. Dr. Cooper reports grants from NIH/NHLBI, Foundation NIH and COPD Foundation,  during the conduct of the study; personal fees from PulmonX, GlaxoSmithKline, NUVAIRA and MGC Diagnostics,  outside the submitted work. Professor Eric Bateman reports personal fees from ALK, AstraZeneca, Boehringer Ingelheim, Menarini, Novartis, Orion, Regeneron and Sanofi outside the submitted work. The authors report no other conflicts of interset in this work.