J Gastroenterol
March 2009
Background: Case reports have linked nonsteroidal antiinflammatory drugs (NSAIDs) to a variety of lesions in the small and large bowel including bleeding, protein loss, strictures, increased intestinal permeability, and NSAID enteropathy. We here review the use of wireless capsule endoscopy to quantitate and assess the nature of the small bowel damage caused by NSAIDs when taken short term and in patients on long-term NSAIDs and COX-2 inhibitors.
Methods: Forty healthy volunteers underwent a baseline capsule endoscopy.
Background: We assessed whether selective granulocyte and monocyte/macrophage adsorption apheresis maintained clinical remission in asymptomatic inflammatory bowel disease (IBD) patients at significant risk of clinical relapse.
Methods: Sixty asymptomatic patients (age 18-70 years) with IBD (in clinical remission) with fecal calprotectin over 250 microg/g (which defines those at risk of clinical relapse with >80% specificity and sensitivity) were recruited for this open-label, prospective, randomized, controlled study. Twenty-nine underwent selective leukocytapheresis, undergoing 5, once weekly, out-patient sessions.
Background & Aims: Nonsteroidal anti-inflammatory drug (NSAID) gastropathy is sufficiently important as to warrant co-administration of misoprostol or proton pump inhibitors or a switch to selective cyclooxygenase (COX)-2 inhibitors. However, the serious ulcer outcome studies suggested that 40% of the clinically significant gastrointestinal bleeding originated more distally, presumably from NSAID enteropathy. We used capsule enteroscopy to study small-bowel damage in patients on long-term NSAIDs and COX-2-selective agents.
View Article and Find Full Text PDFBackground & Aims: It has been variably suggested that nonselective NSAIDs and cyclooxygenase (COX)-2 selective inhibitors aggravate or ameliorate clinical disease activity in patients with inflammatory bowel disease. We assessed the effect of these drugs in patients with inflammatory bowel disease (n = 209) and the possible mechanisms.
Methods: First, patients with quiescent Crohn's disease and ulcerative colitis received the non-NSAID analgesic acetaminophen (n = 26) and the conventional NSAIDs naproxen (n = 32), diclofenac (n = 29), and indomethacin (n = 22) for 4 weeks.
Background & Aims: Conventional acidic nonsteroidal anti-inflammatory drugs frequently cause small bowel inflammation. Diagnosis is largely based on assay of surrogate markers of inflammation in stool, such as fecal calprotectin. However, stool markers are not widely available and the precise nature of this inflammation is uncertain.
View Article and Find Full Text PDFNovartis Found Symp
February 2005
There is a long-standing belief that disruption of the intestinal barrier function may lead to systemic and local intestinal disease. The role of increased intestinal permeability in Crohn's disease is reviewed here. What is not in doubt is that intestinal permeability in patients with Crohn's disease is increased proportional to disease activity; it can be used to predict clinical relapse of disease and prognosis; and a small proportion of first-degree relatives have increased intestinal permeability.
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