Leukotriene E(4) (LTE(4)) is implicated in
asthma pathophysiology and possibly in
chronic obstructive pulmonary disease (
COPD) as one of the causes of persistent bronchoconstriction and mucus hypersecretion. Cigarette smoking stimulates cysteinyl
leukotrienes (CysLTs) production. We investigated whether LTE(4) is equally increased in
asthma and
COPD and whether smoking significantly affects LTE(4) levels. Secondary outcomes involved correlations with inflammatory and functional parameters. We studied 40 patients with
COPD [20 smokers], 40 asthmatics [20 smokers] and 30 healthy subjects [15 smokers]. Spirometry (FEV(1)%
pred., FEV(1)/FVC) was performed, urine was collected for measurement of LTE(4) and
creatinine, induced sputum was collected for differential cell counts and serum for ECP. LTE(4)/
creatinine levels (pg/mg) [mean (sd)] were increased in asthmatic patients compared to
COPD and controls, [125.6(54.5) vs. 54.5(19) vs. 55.9(18.9)pg/mg, respectively, P<0.0001 for
asthma]. Smoking significantly affects LTE(4) levels only in asthmatic patients [164 (48) vs. 87 (26.3), P<0.0001 for smokers]. The only significant correlation was between eosinophils in induced sputum and LTE(4)/
creatinine levels in asthmatics. In conclusion, patients with
asthma presented higher LTE(4) values compared to normals and patients with
COPD. Smoking significantly affects LTE(4) values only in asthmatics indicating a different underlying CysLTs inflammatory process in this condition.