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Thorax 58:585-588 doi:10.1136/thorax.58.7.585
  • Chronic obstructive pulmonary disease

Exhaled leukotrienes and prostaglandins in COPD

  1. P Montuschi1,
  2. S A Kharitonov2,
  3. G Ciabattoni3,
  4. P J Barnes2
  1. 1Department of Pharmacology, School of Medicine, Catholic University of the Sacred Heart, Rome, Italy
  2. 2Department of Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, UK
  3. 3Department of Drug Sciences, G d’Annunzio University, Chieti, Italy
  1. Correspondence to:
    Professor P Montuschi, Department of Pharmacology, School of Medicine, Catholic University of the Sacred Heart, L.go F. Vito, 1-00168 Rome, Italy;
    pmontuschi{at}rm.unicatt.it
  • Accepted 26 March 2003
  • Revised 3 December 2002

Abstract

Background: The role of eicosanoids, including leukotrienes (LTs) and prostaglandins (PGs), in chronic obstructive pulmonary disease (COPD) is uncertain. The aim of this study was to investigate whether eicosanoids are measurable in exhaled breath condensate (EBC), a non-invasive method of collecting airway secretions, in patients with stable mild to moderate COPD, and to show possible differences in their concentrations compared with control subjects.

Methods: LTB4, LTE4, PGE2, PGD2-methoxime, PGF2α, and thromboxane B2 (TxB2) were measured in EBC in 15 healthy ex-smokers, 20 steroid naïve patients with COPD who were ex-smokers, and in 25 patients with COPD who were ex-smokers and who were treated with inhaled corticosteroids. The study was of cross sectional design and all subjects were matched for age and smoking habit.

Results: LTB4 and PGE2 concentrations were increased in steroid naïve (LTB4: median 100.6 (range 73.5–145.0) pg/ml, p<0.001; PGE2: 98.0 (range 57.0–128.4) pg/ml, p<0.001) and steroid treated patients with COPD (LTB4: 99.0 (range 57.9–170.5) pg/ml, p<0.001; PGE2: 93.6 (range 52.8–157.0) pg/ml, p<0.001) compared with control subjects (LTB4: 38.1 (range 31.2–53.6) pg/ml; PGE2: 44.3 (range 30.2–52.1) pg/ml). Both groups of patients had similar concentrations of exhaled LTB4 (p=0.43) and PGE2 (p=0.59). When measurable, LTE4 and PGD2-methoxime concentrations were similar in COPD patients and controls, whereas PGF2α concentrations were increased in the former. TxB2-LI was undetectable in any of the subjects.

Conclusions: There is a selective increase in exhaled LTB4 and PGE2 in patients with COPD which may be relatively resistant to inhaled corticosteroid therapy.

Footnotes

  • This work was performed at Imperial College School of Medicine at the National Heart and Lung Institute, Department of Thoracic Medicine, London, UK.