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Aspirin Intolerance (aspirin + intolerance)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Impact of Aspirin Intolerance on Outcomes of Sinus Surgery,

THE LARYNGOSCOPE, Issue 5 2007
Jamie L. Robinson MD
Abstract Objectives: To compare objective and quality of life (QOL) outcomes after endoscopic sinus surgery (ESS) in aspirin (ASA)-tolerant patients and ASA-intolerant patients over intermediate and long-term follow-up. Study Design: Prospective analysis of a cohort of patients with chronic rhinosinusitis. Methods: Preoperative computed tomography (CT), pre- and postoperative endoscopy, and two validated disease specific QOL instruments, the Rhinosinusitis Disability Index (RSDI) and Chronic Sinusitis Survey (CSS), were collected. Differences in the proportions of patients who improved were analyzed using Pearson's chi-square and Fisher's exact test. Results: Nineteen ASA-intolerant patients and 104 ASA-tolerant patients were followed for a mean of 17.7 months. Patients with ASA intolerance had significantly worse preoperative CT (P < .0001) and endoscopy scores (P < .0001). After ESS, 57% to 74% of patients improved on endoscopy scores, 63% to 71% improved on the RSDI, and 58% to 73% improved on the CSS; improvement did not significantly differ by ASA status. Conclusions: Similar proportions of ASA-tolerant and ASA-intolerant patients showed improvement on endoscopy and QOL measures after ESS. [source]

What do we know about the genetics of aspirin intolerance?

JOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 5 2008
N. S. Palikhe MPharm
Summary Although acetylsalicylic acid is prescribed for a broad range of diseases, it can induce a wide array of clinically recognized hypersensitivity reactions, including aspirin-intolerant asthma (AIA) with rhinitis and aspirin-intolerant urticaria (AIU) with anaphylaxis. Altered eicosanoid metabolism is the generally accepted mechanism of aspirin intolerance; the overproduction of cysteinyl leucotrienes has been suggested to play a causative role in both AIA and AIU. Genetic markers suggested for AIA include HLA-DPBI*0301, leucotriene C4 synthase (LTC4S), ALOX5, CYSLT, PGE2, TBXA2R and TBX21. Similarly, HLA-DB1*0609, ALOX5, FCER1A and HNMT have been identified as possible genetic markers for AIU. An additional low-risk genetic marker for AIA is MS4A2, which encodes the beta-chain of FCER1. Other single and sets of two or more interacting genetic markers are currently being investigated. Analyses of the genetic backgrounds of patients with AIA and AIU will promote the development of early diagnostic and therapeutic interventions, which may reduce the incidence of AIA and AIU. [source]

Association of angiotensin I-converting enzyme gene polymorphisms with aspirin intolerance in asthmatics

CLINICAL & EXPERIMENTAL ALLERGY, Issue 11 2008
T-H. Kim
Summary Background Aspirin-intolerant asthma (AIA) refers to the development of bronchoconstriction in asthmatic individuals following the ingestion of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs). Angiotensin I-converting enzyme (ACE), a membrane-bound peptidase present in the lung, plays a pivotal role in the metabolism of the endogenous peptides involved in the pathogenesis of asthma. Methods We screened a Korean asthma cohort (581 asthmatics including 81 aspirin-intolerant asthmatics and 231 aspirin-tolerant asthmatics, and 181 normal controls) for four single nucleotide polymorphisms (SNPs; ,262 A>T and ,115 T>C in the 5,-flanking region and +5467 T>C [Pro450Pro] and+11860 A>G [Thr776Thr] in the coding region) and one ins/del (+21288 CT) in the ACE gene. Results None of the SNPs or haplotypes showed any association with the development of asthma, but they were significantly associated with the risk of AIA. Logistic regression indicated that the frequency of the rare alleles of ,262 A>T and ,115 T>C was higher in subjects with AIA than in subjects with aspirin-tolerant asthma (ATA) (P=0.003,0.01, P corr=0.015,0.05). Subjects homozygous for the rare alleles of ,262 A>T and ,115 T>C showed a greater decline in forced expiratory volume in 1 s (FEV1) after aspirin provocation than those homozygous for the common alleles (P<0.05). A luciferase reporter assay indicated that ACE promoters containing the rare ,262 A>T allele possessed lower activity than did those containing the common allele (P=0.009). In addition, ACE promoters bearing the rare ,115 T>C allele had no luciferase activity. DNA,protein binding assays revealed a band containing the ACE promoter region (including ,262 A) and a protein complex. Conclusion The ,262 A>T polymorphism in the promoter of the ACE gene is associated with AIA, and the rare allele of ,262 A>T may confer aspirin hypersensitivity via the down-regulation of ACE expression. [source]