Endogenous and exogenous
prostaglandins mobilize gastroduodenal mucosal defenses which are compromised by inhibition of
prostaglandin synthesis with non-steroidal anti-inflammatory drugs (
NSAIDS). There is some evidence, conversely, that stimulation of endogenous
prostaglandin synthesis by increasing precursor availability by dietary enrichment or by provoking its release may increase mucosal integrity. However, there are also non-
prostaglandin defense mechanisms which can be elicited even when
prostaglandin synthesis is profoundly depressed. Most (but not all) evidence suggests that
gastric ulcer patients have deficient
prostaglandin synthesis, though it is not clear whether this is a primary or secondary defect and the evidence on
duodenal ulcer patients is incoherent.
Prostaglandin analogues heal both
gastric ulcers and
duodenal ulcers, mainly as a result of
acid inhibition. There is suggestive, but not conclusive, evidence that subsequent relapse may be retarded.
Misoprostol has obtained a licensed indication for the prevention of
NSAID-induced
peptic ulcer on the basis of studies showing a reduced development of
peptic ulcers and erosions over 4-8 weeks, implying that deficient endogenous
prostaglandin levels can be replaced by exogenous administration.