Inhaled clindamycin in CF patients with chronic infection with Pseudomonas

Austin Bassett Thompson, Paul Henry Sammut, C. G. Judy, A. Floreani, D. Acquazzino, S. I. Rennard, John Louis Colombo

Research output: Contribution to journalArticle

Abstract

Purpose: Clindamycin has been demonstrated, in vitro, to inhibit production of Pseudomonas elastase, an important virulence factor. The purpose of this study was to determine whether inhaled clindamycin can modulate airway inflammation in CF patients chronically infected with Pseudomonas. Methods: Clindamycin was inhaled at a dose of 300 mg bid for 14 days by 5 CF patients with previously documented Pseudomonas infections and moderately severe airway obstruction. Spirometry, clinical history, and expectorated sputum were obtained before therapy and after 2 weeks of therapy. The sputum was mixed with equal volumes of dithiothrietol rocked in a warm water bath for 20 min, and samples were aliquoted for cell counts and quantitative culture of Pseudomonas. The sputum was strained through gauze, centrifuged (5000 rpm, 5 min), and cell differentials were determined for 300 cells after staining cytocentrifuge preparations with Diff-Quik. Results: No changes in spirometry, clinical symptoms or the number of Pseudomonas CFU's per ml sputum were observed over the treatment period. The number of sputum neutrophils before ranged from 13.4-195×106/ ml. The number of neutrophils fell (mean±SEM, 83.8±42.0 to 13.0±4.1, p=0.04) after treatment. Conclusions: Inhaled clindamycin caused a fall in the inflammatory cell burden of the lower respiratory tract as sampled by expectorated sputum, without causing a fall in the burden of Pseudomonas. The study period may have been too short to detect possible improvement in spirometry, but as measured by spirometry, inhaled clindamycin was well tolerated in this small number of patients. Clinical Implications: Non-traditional uses of antibiotics, aimed at modulating lower respiratory tract inflammation, may be of value for the treatment of CF.

Original languageEnglish (US)
JournalChest
Volume110
Issue number4 SUPPL.
StatePublished - Oct 1 1996

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Pseudomonas Infections
Clindamycin
Sputum
Pseudomonas
Spirometry
Respiratory System
Neutrophils
Inflammation
Therapeutics
Pancreatic Elastase
Virulence Factors
Airway Obstruction
Baths
Cell Count
Staining and Labeling
Anti-Bacterial Agents
Water

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Thompson, A. B., Sammut, P. H., Judy, C. G., Floreani, A., Acquazzino, D., Rennard, S. I., & Colombo, J. L. (1996). Inhaled clindamycin in CF patients with chronic infection with Pseudomonas. Chest, 110(4 SUPPL.).

Inhaled clindamycin in CF patients with chronic infection with Pseudomonas. / Thompson, Austin Bassett; Sammut, Paul Henry; Judy, C. G.; Floreani, A.; Acquazzino, D.; Rennard, S. I.; Colombo, John Louis.

In: Chest, Vol. 110, No. 4 SUPPL., 01.10.1996.

Research output: Contribution to journalArticle

Thompson, AB, Sammut, PH, Judy, CG, Floreani, A, Acquazzino, D, Rennard, SI & Colombo, JL 1996, 'Inhaled clindamycin in CF patients with chronic infection with Pseudomonas', Chest, vol. 110, no. 4 SUPPL..
Thompson AB, Sammut PH, Judy CG, Floreani A, Acquazzino D, Rennard SI et al. Inhaled clindamycin in CF patients with chronic infection with Pseudomonas. Chest. 1996 Oct 1;110(4 SUPPL.).
Thompson, Austin Bassett ; Sammut, Paul Henry ; Judy, C. G. ; Floreani, A. ; Acquazzino, D. ; Rennard, S. I. ; Colombo, John Louis. / Inhaled clindamycin in CF patients with chronic infection with Pseudomonas. In: Chest. 1996 ; Vol. 110, No. 4 SUPPL.
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abstract = "Purpose: Clindamycin has been demonstrated, in vitro, to inhibit production of Pseudomonas elastase, an important virulence factor. The purpose of this study was to determine whether inhaled clindamycin can modulate airway inflammation in CF patients chronically infected with Pseudomonas. Methods: Clindamycin was inhaled at a dose of 300 mg bid for 14 days by 5 CF patients with previously documented Pseudomonas infections and moderately severe airway obstruction. Spirometry, clinical history, and expectorated sputum were obtained before therapy and after 2 weeks of therapy. The sputum was mixed with equal volumes of dithiothrietol rocked in a warm water bath for 20 min, and samples were aliquoted for cell counts and quantitative culture of Pseudomonas. The sputum was strained through gauze, centrifuged (5000 rpm, 5 min), and cell differentials were determined for 300 cells after staining cytocentrifuge preparations with Diff-Quik. Results: No changes in spirometry, clinical symptoms or the number of Pseudomonas CFU's per ml sputum were observed over the treatment period. The number of sputum neutrophils before ranged from 13.4-195×106/ ml. The number of neutrophils fell (mean±SEM, 83.8±42.0 to 13.0±4.1, p=0.04) after treatment. Conclusions: Inhaled clindamycin caused a fall in the inflammatory cell burden of the lower respiratory tract as sampled by expectorated sputum, without causing a fall in the burden of Pseudomonas. The study period may have been too short to detect possible improvement in spirometry, but as measured by spirometry, inhaled clindamycin was well tolerated in this small number of patients. Clinical Implications: Non-traditional uses of antibiotics, aimed at modulating lower respiratory tract inflammation, may be of value for the treatment of CF.",
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AU - Rennard, S. I.

AU - Colombo, John Louis

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AB - Purpose: Clindamycin has been demonstrated, in vitro, to inhibit production of Pseudomonas elastase, an important virulence factor. The purpose of this study was to determine whether inhaled clindamycin can modulate airway inflammation in CF patients chronically infected with Pseudomonas. Methods: Clindamycin was inhaled at a dose of 300 mg bid for 14 days by 5 CF patients with previously documented Pseudomonas infections and moderately severe airway obstruction. Spirometry, clinical history, and expectorated sputum were obtained before therapy and after 2 weeks of therapy. The sputum was mixed with equal volumes of dithiothrietol rocked in a warm water bath for 20 min, and samples were aliquoted for cell counts and quantitative culture of Pseudomonas. The sputum was strained through gauze, centrifuged (5000 rpm, 5 min), and cell differentials were determined for 300 cells after staining cytocentrifuge preparations with Diff-Quik. Results: No changes in spirometry, clinical symptoms or the number of Pseudomonas CFU's per ml sputum were observed over the treatment period. The number of sputum neutrophils before ranged from 13.4-195×106/ ml. The number of neutrophils fell (mean±SEM, 83.8±42.0 to 13.0±4.1, p=0.04) after treatment. Conclusions: Inhaled clindamycin caused a fall in the inflammatory cell burden of the lower respiratory tract as sampled by expectorated sputum, without causing a fall in the burden of Pseudomonas. The study period may have been too short to detect possible improvement in spirometry, but as measured by spirometry, inhaled clindamycin was well tolerated in this small number of patients. Clinical Implications: Non-traditional uses of antibiotics, aimed at modulating lower respiratory tract inflammation, may be of value for the treatment of CF.

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