The clinically beneficial effects of AD on nasal and bronchial symptoms occurred only in the patients with AIA.

Chronic rhinosinusitis (CRS) is a multifactorial disease of the upper airways with a high prevalence (approximately 11%) in the general population. Different immune and inflammatory mechanisms are involved in its pathogenesis. Alterations in the arachidonic acid pathway (leading to an imbalanced production of eicosanoids) have been linked to the pathophysiology of different diseases especially nasal polyposis, asthma, and aspirin-exacerbated respiratory disease. Furthermore, viral and bacterial infections have been identified as important factors amplifying the pro-inflammatory reactions in these pathologies. This review summarizes the impact of an imbalance in the eicosanoid pathway and the effect of Staphylococcus aureus enterotoxins on the regulation of the pro-inflammatory network in CRS and their translation into disease severity.

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Corresponding author's email: m.sk@op.plRationale Several open trials have shown good clinical results of aspirin desensitization in aspirin-induced asthma (AIA). The mechanisms of action of aspirin -in this respect -has not been ascertained and it could result just from its potent anti-inflammatory activity. We, therefore, compared clinical and biochemical responses to chronic aspirin desensitization in 20 patients with AIA and 14 with aspirin-tolerant asthma (ATA), all with chronic rhinosinusitis and nasal polyposis, in a double-blind, placebo-controlled study. We investigated some indices of metabolism of eicosanoids, known to participate in pathogenesis of AIA. Method In all patients oral aspirin challenge confirmed or excluded aspirin hypersensitivity. Twelve patients with AIA and 6 with ATA were randomly assigned to aspirin (624 mg once daily for 6 months), whereas 8 with AIA and 6 with ATA to placebo administrated once daily for 6 months. Nasal symptoms, questionnaires [sino-nasal outcome test (SNOT20), Asthma Control Questionnaire (ACQ)], spirometry parameters, peak expiratory flow (PEF), peak nasal inspiratory flow (PNIF) and blood eosinophilia were also measured on monthly basis for 6 months. Urinary leukotriene E (LTE ) and the stable plasma prostaglandin (PG) D metabolite, 9alpha,11beta-PGF were evaluated at 4 4 2 2, baseline and after 1, 3, 5 and 6 months. ResultsOnly AIA patients receiving aspirin reported improvement in sense of smell (p=0.045), reduced sneezing (p=0.04) and rhinorrhea (p=0.02). Their SNOT20 and ACQ scores decreased (p=0.04 and 0.008, respectively) and PNIF values increased (p=0.045). These effects were not observed in any other group studied. Median LTE in AIA patients increased after 6 months of chronic aspirin desensitization as compared 4 to AIA patients taking placebo (p=0.06), whereas plasma 9alpha,11beta-PGF showed no changes.2 Conclusions The results of our study suggest that the positive clinical effect of aspirin desensitization on nasal and bronchial symptoms is specific only for patients with AIA, but it is not observed in ATA patients, subjected to the same regimen. Chronic aspirin desensitization may be associated with an increased production of LTE , but not 9alpha,11beta-PGF . 4 2 This abstract is funded by: none Am J Respir Crit Care Med 183;2011:A1307 Internet address: www.atsjournals.org Online Abstracts Issue