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Urinary leukotriene E 4 and 11‐dehydrothromboxane B 2 in patients with aspirin‐sensitive asthma
Author(s) -
Oosaki R.,
Mizushima Y.,
Mita H.,
Shida T.,
Akiyama K.,
Kobayashi M.
Publication year - 1997
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.1997.tb01032.x
Subject(s) - aspirin , leukotriene e4 , asthma , medicine , urinary system , pathogenesis , leukotriene , gastroenterology , immunology
The objective of this study was to define the participation of cysteinyl leukotrienes (LTs) or thromboxane A 2 in the pathogenesis of aspirin‐sensitive asthma (ASA). Leukotriene E 4 (LTE 4 ) and 11‐dehydrothromboxane B 2 (11DTXB 2 ) values in spot urine were measured in 22 asthmatics with a history of aspirin sensitivity and in 17 without such a history of aspirin‐sensitive asthma [NASA]) in the outpatient clinic. The urinary LTE 4 value was significantly higher in ASA patients than in NASA (340±47 vs 65±15 pg/mg·cr, P <0.001), but there was no significant difference in urinary 11DTXB2 between the two groups (891±77 vs 657±90 pg/mg·cr). A high value of LTE4 was not associated with type of asthma, severity of disease, oral prednisolone treatment, sex, or age. A higher value of 11DTXB 2 was observed in the atopic type than the nonatopic type in ASA (1086±111 vs 697±147 pg/mg·cr, P<0.05). No correlation was observed between urinary LTE 4 and 11DTXB 2 in either ASA or NASA. In conclusion, LTs may play an important role in the pathogenesis of ASA, and TXA 2 in the pathogenesis of the atopic type in ASA.