Abstract
RATIONALE: Patients with AERD can tolerate cyclooxygenase-2 (COX-2) inhibitors whereas cyclooxygenase-1 (COX-1) inhibitors induce symptoms. Since prostaglandin E2 (PGE2) abrogates these symptoms, thought to be caused by elevated cysteinyl leukotriene (CysLT) production, we hypothesised that there is a deficiency of PGE2 production reflecting absent/reduced COX-2 activity in patients with AERD compared to aspirin-tolerant (ATOL) individuals. To address this we developed an ex vivo model of AERD.
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