What prostaglandin product is decreased by COX inhibitors in patients with AERD?

In patients with Aspirin-Exacerbated Respiratory Disease (AERD), the inhibition of cyclooxygenase (COX) enzymes by COX inhibitors leads to a decrease in the production of Prostaglandin E2 (PGE2).

PGE2 is a significant prostaglandin in the airway, playing a critical role in regulating inflammatory responses, bronchial constriction, and mucus production. In AERD, there is an underlying imbalance in the arachidonic acid pathway, where the leukotriene pathway becomes overactive and contributes to asthma symptoms and respiratory distress. COX inhibitors block the conversion of arachidonic acid into prostaglandins, particularly affecting the synthesis of PGE2.

This reduction in PGE2 levels can exacerbate the symptoms associated with AERD, as it diminishes the anti-inflammatory effects that PGE2 may have provided. As such, understanding the role of PGE2 in this context is vital for managing patients with AERD, especially when considering treatment options involving COX inhibitors.