The eosinophilic infiltration in the nasosinusal polyp associated with intolerance to aspirin is predominant feature. Several mediators play a role in the migration of the eosinophils to the tissues. The IA may be due to overexpression of leukotrienes in genetically susceptible subjects. AIM: The purpose of this study was to evaluate the cytokine pattern and HLA-A, B and DR typing in subjects with PNS tolerant and intolerants to aspirin. STUDY DESIGN: A transverse cohort study. MATERIAL AND METHOD: was conducted on 45 patients: 15 patients suffering from eosinophilic PNS and aspirin tolerance (group TA); 15 from eosinophilic PNS associated with aspirin intolerance, the latter manifested by bronchospasm (group IA), and 15 without PNS who had nasal septum deviation (control group). Cytokine pattern (IL-2; IL-4; IL-5; IL-6; IL-8; IL-10; IFN-gamma and TNF-alpha) was evaluated in samples from the nasal polyp or midlle turbinate mucosa (control group) of the patients using reverse transcription-polymerase chain reaction (RT-PCR). HLA-A, B and DR typing was performed using the serum microcytotoxicity test or by DNA amplification using polymerase chain reaction (PCR). RESULTS: mRNA expression for interleukines 4, 5, 6, 8, 10, IFN-gamma and TNF-alpha was similar in the three groups. mRNA expression for IL-2 was associated with IA. Patients with antigens A11, B49, DR15 and DR13 had a higher likelihood of developing PNS not-related to intolerance to Aspirin, whereas patients with DR17 had a higher likelihood of developing PNS associated with intolerance to Aspirin (Aspirin Triad). CONCLUSION: PNS associated with intolerance to Aspirin (Aspirin Triad) shows a significant association with HLA- DR17 and IL-2, suggesting a TH1-lymphocyte-activation pattern.
nasal polyps; aspirin; cytokines; HLA antigen
