Correlation among urinary eosinophil protein X, leukotriene E₄, and 11‐dehydrothromboxane B₂ in patients with spontaneous asthmatic attack

Abstract

Various kinds of cells and their mediators are thought to be involved in the pathogenesis of bronchial asthma. However, changes in each mediator or relationship among mediators during an asthmatic attack have not been well documented. In this study, to clarify whether eosinophil protein X (EPX) is a marker which is distinct from leukotriene E4 (LTE4), or 11-dehydrothromboxane B2 (11DTXB2), we measured the urinary excretion of EPX, LTE4, and 11DTXB2 in 14 asthmatics who were admitted to the hospital with either an acute asthmatic attack or status asthmaticus. These patients included eight atopic and six non-atopic types of bronchial asthma, with a median age of 34.0 years. Urinary excretion of EPX was significantly high on admission with the asthmatic attack, and returned to control levels 175 [122 -384] microg/day when the patients were in the improved state (1036-317 microg/day, P < 0.01). Similar findings were observed in LTE4 (155-59 ng/day, P < 0.01) and 11DTXB2 (991-442ng/day, P<0.01). No significant differences in values were observed between atopic and non-atopic types of asthma in all three substances. When the individual data during the attack state were analysed, a significant correlation was observed between changes (%) in urinary EPX and those in urinary LTE4, but no such relationship was observed between changes (%) in urinary EPX and those in urinary 11DTXB2. These results suggest that measuring urinary EPX levels may be a useful marker for the understanding and management of the disease.

CD203c expression on human basophils is associated with asthma exacerbation

“…2 It was also found that human basophils produce high levels of IL-4 in the lung after segmental allergen challenge. 3 Oosaki et al 4 reported that in patients with spontaneous asthma attacks, urinary excretions of eosinophil protein X, leukotriene E4, and 11-dehydrothromboxane B2 significantly increase during the attack and return to control levels in the improved phase. In addition, Nakano et al 5 showed that patients admitted to a hospital because of nonresolving asthma exacerbation had higher plasma levels of C3a, a potent proinflammatory mediator, than patients discharged immediately after the exacerbation or patients with stable asthma.…”

Clinical features of asthmatic patients with increased urinary leukotriene E4 excretion (hyperleukotrienuria)Involvement of chronic hyperplastic rhinosinusitis with nasal polyposis

“…6,7 Previous studies have shown that the U-LTE4 concentration is useful in demonstrating cys-LT release in vivo during allergen challenge 8,9 and acute exacerbation of asthma. 10,11 Moreover, even in clinically stable conditions, basal urinary excretion levels of LTE4 in patients with aspirin-intolerant asthma (AIA) are significantly higher than those in patients with aspirin-tolerant asthma (ATA). 12,13 The cellular source of cys-LTs is as yet unknown, but it possibly includes eosinophils and mast cells.…”

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

“…The relationship between urinary LTE 4 and 11DTXB 2 in the pathogenesis of asthma has been reported by several investigators; [2][3][4][5]8,11,13,20 because of the instability of CysLTs and TXA 2 , the end-products of the cascade were determined. However, most studies have been Fig.…”

“…Moreover, increased production of CysLTs in asthmatic patients in vivo has been observed in several studies. [1][2][3][4][5]11,12 A potent bronchoconstrictor, TXA 2 is generated from arachidonic acid by cyclooxygenase. Enhanced TXA 2 release has also been reported in asthmatic patients after allergen challenge.…”