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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1996-3-6
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pubmed:abstractText |
Bronchial overproduction of leukotrienes and inhibition of prostaglandin synthesis are involved in the pathogenesis of aspirin-induced asthma. We investigated whether inhaled prostaglandin E2 (PGE2) attenuates the response to bronchial challenge with lysine acetylsalicylate (LASA) and the associated increase in urinary leukotriene E4 (u-LTE4) in seven aspirin-sensitive subjects with asthma. Each subject performed two challenges with a single dose of LASA that caused a decrease in FEV1 of 20% or more in a preliminary test, immediately after inhaling 100 micrograms PGE2 in 4 ml saline or placebo, according to a randomized double-blind protocol. FEV1 was recorded at 30-min intervals for 4 h. u-LTE4 was measured by combined high-performance liquid chromatography enzyme immunoassay at 2-h intervals. After placebo, LASA caused an obstructive reaction in all patients, with a maximum decrease in FEV1 of 35 +/- 5% with respect to baseline. u-LTE4 rose from 911 +/- 261 picograms (pg)/mg creatinine at baseline to a maximum value of 2249 +/- 748 after challenge. Inhaled PGE2 provided almost complete protection in all patients. Baseline u-LTE4 was 883 +/- 243 pg/mg creatinine and did not change significantly during the test, reaching a maximum value of 864 +/- 290 (p < 0.05 versus placebo). These results confirm that PGE2 is highly effective in preventing aspirin-induced asthma and suggest that this effect is mediated by inhibition of sulfidopeptide leukotriene production.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aspirin,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Leukotriene E4,
http://linkedlifedata.com/resource/pubmed/chemical/Lysine,
http://linkedlifedata.com/resource/pubmed/chemical/acetylsalicylic acid lysinate
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1073-449X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
153
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
572-5
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8564100-Administration, Inhalation,
pubmed-meshheading:8564100-Adolescent,
pubmed-meshheading:8564100-Adult,
pubmed-meshheading:8564100-Aspirin,
pubmed-meshheading:8564100-Asthma,
pubmed-meshheading:8564100-Bronchial Provocation Tests,
pubmed-meshheading:8564100-Bronchoconstriction,
pubmed-meshheading:8564100-Chromatography, High Pressure Liquid,
pubmed-meshheading:8564100-Dinoprostone,
pubmed-meshheading:8564100-Double-Blind Method,
pubmed-meshheading:8564100-Female,
pubmed-meshheading:8564100-Forced Expiratory Volume,
pubmed-meshheading:8564100-Humans,
pubmed-meshheading:8564100-Leukotriene E4,
pubmed-meshheading:8564100-Lysine,
pubmed-meshheading:8564100-Male,
pubmed-meshheading:8564100-Middle Aged
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pubmed:year |
1996
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pubmed:articleTitle |
Inhaled PGE2 prevents aspirin-induced bronchoconstriction and urinary LTE4 excretion in aspirin-sensitive asthma.
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pubmed:affiliation |
Institute of Respiratory Diseases, University of Siena, Italy.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Randomized Controlled Trial,
Research Support, Non-U.S. Gov't
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