Chronic use of non-
salicylate NSAIDs causes in most individuals an asymptomatic enteropathy involving the small bowel, particularly its distal part. This enteropathy is characterised by an increase in intestinal permeability and a mild mucosal
inflammation.
Hypoalbuminemia and
iron deficiency may occur. In addition, non-
salicylate NSAIDs may cause focal lesions of the small intestine. Ulcerations and
ulcers, that can be accidentally discovered during an ileoscopy, may cause acute or chronic
bleeding. Deep
ulcers may provoke sudden
peritonitis. Small bowel diaphragms are rare fibrotic lesions, specifically associated with the use of non-
salicylate NSAIDs or
salicylates (duodenal diaphragms only).
NSAID use is not associated with a constant toxicity on colonic mucosa.
NSAID-induced colonic
ulcers and diaphragms are rare. In patients with
colonic diverticulosis,
NSAID intake is a risk factor for severe attacks of
diverticulitis. Acute or chronic use of non-
salicylate NSAIDs increases the risk for
ischemic colitis and flare-ups of
inflammatory bowel disease. De novo
colitis caused by non-
salicylate NSAIDs are rare. The definite diagnosis of this entity relies on the absence of recurrence of
colitis in the 2-3 following years. Such a recurrence would lead to the post-hoc diagnosis of first attack of
inflammatory bowel disease triggered by
NSAID use. Experimental data suggest that selective
COX-2 inhibitors do not alter constantly mucosa of the small intestine. Pilot epidemiological works suggest that severe intestinal lesions are less frequent in association with
COX-2 inhibitor use than in association with conventional
NSAIDs. However, COX-2 appears as playing a beneficial role in mucosal healing, and it seems that
COX-2 inhibitors, like conventional
NSAIDs, may trigger flare-ups of
inflammatory bowel disease.