A team from Nottingham, England, and Rahway, New Jersey, investigated whether rofexicob, a COX-2 inhibitor, hinders the synthesis of gastric mucosal prostaglandin.
|Effect of treatment on synthesis of gastric mucosal prostaglandin:|
Naproxen: decrease of 65%
Rofexicob: increase of 18%
24 healthy, non-smoking Helicobacter pylori-negative volunteers were randomized to one of two separate concurrent blinded crossover studies.
16 volunteers received rofecoxib, 50 mg once daily, for 5 days in one treatment period and placebo in the other.
8 volunteers similarly received naproxen, 500 mg twice daily, and placebo.
On Day 5 of each period, antral mucosal prostaglandin E2 (PGE2) synthesis was measured by radioimmunoassay after vortexing for 3 minutes. Whole blood COX-1 activity was measured as serum thromboxane (TXB)2- and COX-2 activity as lipopolysaccharide (LPS)-induced PGE2.
The team found that, compared to placebo, naproxen decreased gastric mucosal PGE2 synthesis by 65% in contrast to an 18% increase after rofecoxib.
Naproxen also significantly inhibited both serum TXB2 by 94% and LPS-induced PGE2 production by 77%, but rofecoxib only inhibited COX-2-dependent LPS-induced PGE2 (by 79%).
Nicholas Wight, of the University Hospital, Nottingham, concluded on behalf of the group, "Rofecoxib (50 mg) lacked naproxen's ability to reduce the availability of gastro-protective prostaglandins."