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Pathogenesis of nonsteroidal antiinflammatory drug-induced asthma Seung-Hyun Kim and Hae-Sim Park Abbreviations Purpose of review To summarize recent findings related to the pathogenic 15-HETE 15-hydroxyeicosatetranoic acid AIA aspirin-induced asthma mechanisms of aspirin-induced asthma with emphasis on ALOX5 5-lipoxygenase molecular genetic mechanisms. ALOX5AP 5-lipoxygenase activating protein ASA acetyl salicylic acid Recent findings ATA aspirin-tolerant asthma The overproduction of cysteinyl leukotrienes with the COX-2 cyclooxygenase 2 Cys-LT cysteinyl leukotriene increased expression of cysteinyl leukotriene receptor EP2 prostaglandin E receptor subtype 2 1 (CYSLTR1) is a consistent finding in aspirin-induced FEV1 forced expiratory volume in 1 s LTC4S leukotriene C4 synthase asthma patients. Recent data have suggested a NSAID nonsteroidal antiinflammatory drug dysregulation of cyclooxygenase-2 and prostaglandin E , SNP single nucleotide polymorphism TBX21 T-box expressed in T cells increased levels of 15-hydroxyeicosatetranoic acid, and TBXA2R thromboxane A2 receptor decreased lipoxin generation as characteristics of the condition. The HLA allele DPB1 0301 was documented as 2006 Lippincott Williams & Wilkins a strong genetic marker for susceptibility in an Asian 1528-4050 population. Leukotriene C4 synthase has been established as a key genetic determinant of aspirin-induced asthma, but recent studies have demonstrated that several single Introduction nucleotide polymorphisms in the promoters of Aspirin (acetyl
Current Opinion in Allergy and Clinical Immunology – Wolters Kluwer Health
Published: Feb 1, 2006
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