Abstract

OBJECTIVE: This study aims to examine the regulation of cyclooxygenase-2 (COX-2) enzyme which is an inducible isoform of cyclooxygenase to elucidate the difference of arachidonic acid metabolism and to compare the gene expression levels of COX-2 in aspirin-sensitive and tolerant patients.

METHODS: This study was conducted on 19 aspirin-tolerant patients with nasal polyposis, 14 aspirin-sensitive patients with nasal polyposis and nine patients (control group) who underwent septal surgery and did not have chronic rhinosinusitis and nasal polyps, who were admitted to the Ear-Nose-Throat Clinic of Bakirkoy Dr. Sadi Konuk Training and Research Hospital between June 2006 and March 2009, were treatment-naiive or it had been six months since the last treatment they received. The COX-2 gene expression was checked for its prevalence and severity in the cytoplasm of inflammatory cells using the immunohistochemical method on the specimens collected from the patients.

RESULTS: The COX-2 prevalence phases of the aspirin-sensitive group was found to be significantly lower compared to the aspirin-tolerant and control patients (p=0.014; p=0.002). No significant differences were observed in the COX-2 prevalence phases between the aspirin-tolerant and control group patients (p=0.324; p>0.05). The COX-2 severity of the aspirin-tolerant group was significantly lower than the aspirin-tolerant and control patients (p=0.036; p=0.022). No significant differences were observed between the COX-2 severities of aspirin-tolerant and control group patients (p=0.852; p>0.05).

CONCLUSION: In our study, we found that the COX-2 gene expression was low in the aspirin-sensitive patients. This finding supports the hypothesis on the inhibition of the COX-1 enzyme following aspirin and other nonsteroidal antiinflammatory drug intake, the consequent inadequate regulation of the COX-2 enzyme in aspirin-sensitive patients and the reduction in the PGE2 synthesis. However, there is a need for further studies to shed light on the enzyme regulation mechanisms particularly to keep the inadequate regulation of COX-2 responsible per se for this pathogenesis.