Prostaglandins are synthesized from arachidonic acid catalyzed by the enzyme cyclooxygenase. Prostaglandins, particularly the E series, have biologic properties that can enhance microvascular permeability with subsequent edema, vasodilatation and induction of pain. In IBD, there is in increased level of prostaglandin production. Elevated levels of prostaglandins are found in the stool, venous blood and rectal mucosa in IBD. Prostaglandin levels in IBD in mucosa, serum or rectal dialysates correlate with disease activity. Successful medical management results in reduction in prostaglandin levels.
There is some evidence, however, that contradicts the role of prostaglandins as proinflammatory mediators in IBD. The use of potent cyclooxygenase inhibitors, indomethacin and other nonsteroidal anti-inflammatory drugs (NSAIDs), results in both a decrease in prostaglandin synthesis and in clinical improvement in rheumatoid arthritis and other inflammatory diseases. However, NSAIDs have no role in the medical management of IBD. Small trials of indomethacin administered orally or rectally revealed no improvement in ulcerative colitis. Some reports have shown that both indomethacin and flurbiprofen may cause clinical deterioration despite causing a decrease in prostaglandin production. The failure of NSAIDs to induce clinical improvement in IBD suggests that the secretion of prostaglandin and other inflammatory mediators such as PAE, leukotrienes and proinflammatory cytokines including chemokines, must be inhibited concurrently to reduce tissue injury.
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