Adverse effects of nonsteroidal anti-inflammatory drugs on the colon.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used, and a growing body of evidence suggests that they have adverse effects in the lower gastrointestinal (GI) tract in addition to the well-described toxicity in the upper GI tract. Among NSAID users who develop adverse GI effects, the proportion with lower GI events is as high as 40%. Most of the available evidence is taken from case-control studies and case reports; no large, randomized, placebo-controlled study has specifically set out to determine the magnitude of NSAID toxicity on the colon.

Clinical features affecting final adult height in patients with pediatric-onset Crohn's disease.

Background: Growth failure is a recognized complication of pediatric-onset Crohn's disease, but there are few data on final adult height.

Objective: Our purpose with this work was to determine adult height and the clinical features that influence long-term growth impairment.

Methods: We retrospectively studied 123 patients with Crohn's disease (65 male and 58 female) who had reached adult height.

Intestinal inflammation-induced growth retardation acts through IL-6 in rats and depends on the -174 IL-6 G/C polymorphism in children.

Inflammatory diseases frequently impair linear growth. Crohn's disease inhibits growth in up to one third of affected children. In rats with trinitrobenzenesulphonic acid-induced colitis, 40% of growth impairment is attributable to inflammation, with the rest being due to undernutrition.

Interleukin-5 potentiates the growth response of Caco-2 cells to IGF-II: a role in colonic carcinogenesis complicating ulcerative colitis?

Unlabelled: Longstanding ulcerative and Crohn's colitis increases the risk of colorectal cancer (CRC) compared to the general population. Elevated IGF-II mRNA and protein have been found in tumour tissue in sporadic CRC. The association of IGF-II in colitis-related-CRC is unknown.

Cyclooxygenase 2, p53, beta-catenin, and APC protein expression in gastric adenomatous polyps.

Gastric adenomatous polyps are rare findings in upper gastrointestinal endoscopy; however, they are associated strongly with malignant transformation. Few series describe the oncogenic characteristics of gastric adenomas. In the present study, we immunohisto-chemically assessed the expression of cyclooxygenase (COX)-2, beta-catenin, p53, and adenomatous polyposis coli (APC) in paraffin-embedded specimens of 14 gastric adenomas.

Prostaglandin E2 production and T cell function after fish-oil supplementation: response to antioxidant cosupplementation.

Background: Prostaglandin E(2) (PGE(2)) inhibits lymphocyte proliferation and the production of interferon-gamma (IFN-gamma) by peripheral blood mononuclear cells, but the effect of PGE(2) on interleukin 4 (IL-4) production is unclear. Fish oil, which contains eicosapentaenoic and docosahexaenoic acids, inhibits production of PGE(2). The effects of fish oil on lymphocyte proliferation and production of IFN-gamma and IL-4 are unclear and may be influenced by the availability of antioxidants.

Inhibition of tumour necrosis factor-alpha and interleukin 6 production by mononuclear cells following dietary fish-oil supplementation in healthy men and response to antioxidant co-supplementation.

Increased dietary consumption of the n-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic acid (20 : 5n-3; EPA) and docosahexaenoic acid (22 : 6n-6; DHA) is associated with their incorporation into circulating phospholipid and increased production of lipid peroxide metabolites. The relationship between peripheral blood mononuclear cell (PBMC) function, n-3 PUFA intake and antioxidant co-supplementation is poorly defined. We therefore investigated tumour necrosis factor (TNF)-alpha and interleukin (IL) 6 production by PBMC and phospholipid fatty acid composition in plasma and erythrocytes of healthy male subjects (n 16) receiving supplemental intakes of 0.

Gastrointestinal side effects of drugs.

Drugs can have adverse effects on any part of the gastrointestinal (GI) tract from mouth to colon. It is essential that a detailed and accurate drug history is taken in patients presenting with GI complaints. Many drug-induced effects will regress or heal on cessation of treatment.

Delayed puberty associated with inflammatory bowel disease.

Delayed puberty frequently complicates the clinical course of young patients with inflammatory bowel disease, more often in Crohn's disease than ulcerative colitis. Undernutrition has been thought to be the main reason for delayed puberty in these patients. However, puberty may be delayed despite a normal nutritional status.

Fundamental mechanisms of growth failure in inflammatory bowel disease.

Growth failure is common in children with inflammatory bowel disease (IBD) and has been attributed chiefly to undernutrition. Liquid enteral feeding can reverse the calorie deficit and increase growth velocity. The inflammatory process per se may also directly inhibit linear growth.

Endothelin in human inflammatory bowel disease: comparison to rat trinitrobenzenesulphonic acid-induced colitis.

There have been suggestions that endothelins (ET-1, ET-2, ET-3) are involved in the pathogenesis of human inflammatory bowel disease (IBD). Furthermore, the non-selective endothelin receptor antagonist, bosentan, ameliorates colonic inflammation in TNBS colitis in rats. However, no studies have measured the tissue expression and release of endothelins in human IBD in direct comparison to experimental TNBS colitis.

Orlistat: its current status as an anti-obesity drug.

Orlistat is a non-centrally acting anti-obesity agent that acts locally in the gastrointestinal tract to inhibit lipase, an enzyme that is crucial for the digestion of long-chain triglycerides. At the recommended dose of 120 mg three times daily, orlistat inhibits dietary fat absorption by about 30%. Over a 1-year period, obese patients taking orlistat in combination with a hypocaloric diet show a reduction of 2-5 kg over the weight decrease with placebo.

Anorexia in a rat model of colitis: interaction of interleukin-1 and hypothalamic serotonin.

Background And Aims: Anorexia induced by experimental colitis in rats is mediated, in part, by increased release of serotonin (5-HT) from the hypothalamic paraventricular nucleus (PVN). In this model, anorexia is attenuated by treatment with an interleukin-1 (IL)-1 receptor antagonist (ra). However, a functional link between central IL-1 receptors and 5-HT release remains unproven.

Management of growth retardation in the young patient with Crohn's disease.

Linear growth retardation is a major complication of Crohn's disease that occurs in children. It is related both to undernutrition and to direct effects of the inflammatory process on the growth axis. Enteral nutrition (elemental, semi-elemental or polymeric diet) employed as the sole source of nutrition remains a mainstay of treatment of active Crohn's disease because it corrects nutritional deficits, has anti-inflammatory effects, heals mucosal inflammation and stimulates growth.