Division of Pulmonology, Department of Medicine, Stellenbosch University, Cape Town, South Africa.
University of Cape Town Lung Institute, and Division of Pulmonology, Department of Medicine, University of Cape Town, Cape Town, South Africa.
Int J Chron Obstruct Pulmon Dis. 2020 May 11;15:1039-1047. doi: 10.2147/COPD.S219731. eCollection 2020.
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.
肺结核(PTB)与多种慢性肺部疾病有关,包括慢性气流阻塞(AFO)的发展。然而,PTB 后 AFO 的性质、演变和机制尚不清楚。本研究旨在检查接受 PTB 治疗的患者肺生理变化的进展。
对接受门诊治疗的初治肺结核免疫功能正常的健康成年患者进行前瞻性随访,在肺结核诊断时、治疗期间和治疗结束后 2、6、12 和 18 个月进行系列肺生理和定量计算机断层扫描(CT)肺扫描。
49 例患者(中位年龄 26 岁;37.2%为男性)入选,43 例患者进行了研究。在治疗期间,肺容积改善,CT 纤维化评分降低,但 AFO 和气体潴留的特征出现,而大多数患者持续存在的弥散能力(DLco)降低。治疗完成后一年,通过体积描记法观察到总肺容量(TLC)显著增加(中位变化 5.9%预测值,P<0.01),主要由残气量(RV)增加引起(中位变化+19%预测值,P<0.01),但不包括吸气量(IC;P=0.41)。RV/TLC 的变化与治疗后放射性气体潴留的显著进展相关(P=0.04),但与肺气肿评分无关。治疗完成后 1 年,18.6%的患者有残余限制(TLC<80%预测值),16.3%有 AFO,32.6%有气体潴留(RV/TLC>45%),78.6%有降低的 DLco。
单纯的肺量计检查不能完全揭示初次肺结核发作后残留的呼吸损害。治疗后生理变化会继续发展,这些发现表明,在愈合过程中小气道病变的进展可能导致治疗后气体潴留的出现。