کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4212457 | 1280690 | 2007 | 7 صفحه PDF | دانلود رایگان |

SummaryLeukotriene E4 (LTE4) 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 LTE4 is equally increased in asthma and COPD and whether smoking significantly affects LTE4 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 (FEV1% pred., FEV1/FVC) was performed, urine was collected for measurement of LTE4 and creatinine, induced sputum was collected for differential cell counts and serum for ECP.LTE4/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 LTE4 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 LTE4/creatinine levels in asthmatics.In conclusion, patients with asthma presented higher LTE4 values compared to normals and patients with COPD. Smoking significantly affects LTE4 values only in asthmatics indicating a different underlying CysLTs inflammatory process in this condition.
Journal: Respiratory Medicine - Volume 101, Issue 4, April 2007, Pages 826–832