Incidence and pathophysiology of peptic ulcer bleeding

Peptic ulcer accounts for about 50% of all cases of upper gastrointestinal bleeding. Acute mortality may be as high as 14%. Infection with Helicobacter plyori (Hp) and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the predominant risk factors. While the prevalence of Hp in ulcer bleeding is still debated, there is strong evidence that eradication of bacteria reduce the risk of re-bleeding significantly. The use of NSAIDs increases the frequency of ulcer bleeding about four- to sixfold on average. Additional factors such as advanced age, concomitant use of corticosteroids or anticoagulants, prior ulcer complications and co-morbid diseases may further increase the risk of bleeding. Whether or not Hp infection also represents an additive risk factor in NSAID-related bleeding remains to be clarified. The pathophysiologic action of both Hp and NSAIDs is quite complex. Hp promotes the aggressive factor acid and damages several mucosal defence mechanisms by liberating lipopolysaccharide, urease and vacuolating cytotoxin. In NSAID toxicity the cyclo-oxygenase enzymes (COX) have been studied intensively. With the advent of COX-2-selective NSAIDs, the clinical problem of NSAID-induced ulcer bleeding may be markedly reduced or abolished completely.