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Clinical Investigations: BRONCHIECTASIS |

Sputum Elastase in Steady-State Bronchiectasis*

Kenneth W. Tsang, MD, FCCP; Kwok-ning Chan, MD, PhD; Pak-leung Ho, MRCP; Ling Zheng, MD, PhD; Gaik C. Ooi, FRCR; James C. M. Ho, MRCP; Wah-kit Lam, MD, FCCP
Author and Funding Information

*From the University Departments of Medicine (Drs. Tsang, Zheng, J.C.M. Ho, and Lam), Microbiology (Dr. P. Ho), Diagnostic Radiology (Dr. Ooi), and Paediatrics (Dr. Chan), The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong SAR, China.

Correspondence to: Kenneth W.T. Tsang MD (Hons), FCCP, University Department of Medicine, Queen Mary Hospital, Pokfulam, Hong Kong SAR, China; e-mail: kwttsang@hkucc.hku.hk



Chest. 2000;117(2):420-426. doi:10.1378/chest.117.2.420
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Study objectives: To study the correlations between sputum elastase output with clinical and sputum inflammatory and microbial factors in steady-state bronchiectasis.

Design: Prospective recruitment of patients with bronchiectasis (17 women; 48.5 ± 16.5 years old; FEV1/FVC, 1.3 ± 0.6/2.1 ± 0.9) for assessment of 24-h sputum output of elastase, bacteria, leukocytes, interleukin (IL)-1β, IL-8, tumor necrosis factor-α, and leukotriene B4. Clinical variables assessed concomitantly included 24-h sputum volume, lung spirometry, number of lung lobes affected by bronchiectasis, and exacerbation frequency.

Setting: Consecutive recruitment of outpatients (n = 30) in steady-state bronchiectasis.

Measurements and results: Twenty-four-hour sputum elastase output correlated with 24-h sputum volume (r = 0.79, p = 0.0001); number of bronchiectatic lung lobes (r = 0.54, p = 0.0026); percent predicted FEV1 (r = −0.48, p = 0.0068); percent predicted FVC (r = −0.49, p = 0.001); and leukocyte output (r = 0.75, p = 0.0001). There was no correlation between the sputum output of bacteria with either inflammatory or enzymatic factors (p > 0.05).

Conclusion: Our data highlight the importance of elastase and the possibility of independent roles for enzymatic, inflammatory, and microbial components in the pathogenesis of bronchiectasis. Further research on novel therapy targeting each of these components should be pursued.

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