Aspirin was commercialized more than a 100 years ago. Today, this compound is still widely prescribed, and new mechanisms of action and indications are being tested. Inhibition of
cyclooxygenase (COX)-1 and COX-2 by
aspirin or its related compounds, nonsteroidal antiinflammatory drugs (
NSAIDs), has been associated with both adverse and beneficial effects in the gastrointestinal (GI) tract. Inhibition of COX-1 has been linked to GI adverse effects. Adverse effects of
NSAIDs and
aspirin in the upper GI tract include
esophagitis, peptic ulcer, peptic ulcer complications, and death. Effective preventive
therapies are available that have been associated with a progressive decline in the rate of hospitalization due to upper GI complications.
NSAIDs and
aspirin can also damage the small bowel and the colon.
NSAID enteropathy is frequent and in most cases subclinical (increased mucosal permeability,
inflammation, erosion,
ulcer). However, more serious clinical outcomes such as
anemia,
bleeding, perforation, obstruction,
diverticulitis, and deaths have also been described. Prevention
therapy of
NSAID damage to the lower GI tract is not well defined. Inhibition of COX-2 by
NSAIDs,
coxibs, or
aspirin seems to provide beneficial effects to the GI tract. Observational studies show that these compounds reduce the risk of both upper and lower GI
cancers. Randomized controlled trials have shown that
aspirin and
coxibs reduce the recurrence rate of
colonic polyps, and long-term cohort studies have shown that
aspirin reduces the risk of
colon cancer time and dose dependently. New studies will have to define the appropriate population that may benefit with these
therapies.