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Urinary leukotriene E 4 in Henoch–Schonlein purpura
Author(s) -
Tsuji Y.,
Abe Y.,
Hisano M.,
Sakai T.
Publication year - 2004
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2004.02029.x
Subject(s) - henoch schonlein purpura , leukotriene e4 , purpura (gastropod) , nephritis , medicine , pathophysiology , leukotriene receptor , urinary system , immunology , gastroenterology , antagonist , leukotriene , receptor , disease , asthma , vasculitis , biology , ecology
Summary Background Children with Henoch–Schonlein purpura (HSP) occasionally have allergic disease. We have previously shown that pranlukast hydrate was effective for purpura in HSP. Pranlukast hydrate is a leukotriene (LT) receptor antagonist; therefore, it is likely that LTs take part in the cause of HSP. Urinary leukotriene E 4 (LTE 4 u) levels are a useful index of whole‐body cysteinyl LT production in vivo . In this study, LTE 4 u was examined in children with HSP. Objective The purpose of this study was to examine the relation between the level of LTE 4 u and the cause of HSP. Methods Eighteen HSP children (six boys and 12 girls) and six healthy children were enrolled. Results LTE 4 u levels in patients with HSP were significantly higher ( P <0.05) at the onset than those in healthy children. Four weeks therapy with pranlukast hydrate lowers LTE 4 u levels in patients with HSP ( P <0.05). There were no differences in LTE 4 u between the group of HSP patients with purpura nephritis and the group of HSP patients without purpura nephritis. Conclusion These results indicate that csyteinyl LTs may play a role in the pathophysiology of purpura in HSP.