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Urinary leukotriene E4 and 11-dehydro-thromboxane B2 excretion in children with bronchial asthma

Authors


Kaori Yoshikawa, Department of Pediatrics, Graduate School of Medicine, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan. Email: kimatan@tj8.so-net.ne.jp

Abstract

Background:  Cysteinyl leukotrienes (CysLTs) and thromboxane (TX) A2 have been implicated in the pathogenesis of bronchial asthma. Urinary leukotriene E4 (LTE4) and 11-dehydro-TXB2 (11DTXB2) levels are often used to assess the production of CysLTs and TXA2. However, few studies have examined the products of these two mediators in the same asthmatic patients. To define the potential roles of CysLTs and TXA2 in the pathogenesis of bronchial asthma in children, their urinary levels were measured in the present study.

Methods:  Urinary LTE4 and 11DTXB2 levels were measured by enzyme immunoassay (EIA) and radioimmunoassay (RIA), respectively. Urine samples from asthmatic children were measured during the stable condition and during an acute attack.

Results:  Urinary LTE4 levels during an acute attack (median 476 pg/mg creatinine; range 191−1100 pg/mg creatinine) and during the stable condition (median 332 pg/mg creatinine; range 128−965 pg/mg creatinine) were significantly higher (P < 0.05) than those of controls (median 233 pg/mg creatinine; range 103−389 pg/mg creatinine). Urinary 11DTXB2 levels during an acute attack and during the stable condition (median 1666 (range 110−5105) and 1009 (range 46−6070) pg/mg creatinine, respectively) were significantly higher (P < 0.05) than those of controls (median 252 pg/mg creatinine; range 41−716 pg/mg creatinine). Comparing different stages of asthma, LTE4 levels during an acute attack were significantly higher (P < 0.05) than during the stable condition; however, there was no difference in urinary TXB2 levels.

Conclusions: The present findings suggest that high levels of CysLTs and TXA2 are associated with the pathogenesis of bronchial asthma. The measurement of urinary LTE4 and 11DTXB2 would be useful in understanding the individual pathogenesis of asthmatic children.

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