mobic and Ulcer

The diagnosis of NSAID-induced colon ulcers is difficult when the distribution or endoscopic findings are not typical. An 83-year-old woman was transferred to our hospital for hemorrhagic diarrhea. Colonoscopy showed multiple ulcers in the entire colon, particularly longitudinal ulcers in the transverse colon. These were unusual for NSAID-induced colopathy, although she had been on meloxicam. However, capsule endoscopy revealed multiple scars and erosions, characteristic of NSAIDs users. The final diagnosis was NSAID-induced enteropathy, and all lesions were in remission after meloxicam discontinuation. We herein emphasize the value of an endoscopic assessment of the entire digestive tract in the diagnosis of NSAID-induced mucosal lesions.

Topics: Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Capsule Endoscopy; Colon; Colonoscopy; Female; Gastrointestinal Hemorrhage; Humans; Intestine, Small; Meloxicam; Thiazines; Thiazoles; Ulcer

Large intestinal ulcers, bleeding and perforation are occasionally due to non-steroidal anti-inflammatory drugs (NSAID). In addition to suppression of prostaglandins synthesis, a number of factors have been implicated, including enterohepatic recirculation, food intake and vascular injury with oxygen free-radical generation. The present study aimed to determine the effect of food intake and the role of oxidative stress in the pathogenesis of intestinal injury induced by oral administration of meloxicam (preferential cyclooxygenase-2 inhibitor) vs. piroxicam (preferential cyclooxygenase-1 inhibitor). Therefore, the activity of oxidative stress-related enzymes such as myeloperoxidase, xanthine oxidase and superoxide dismutase, as well as levels of lipid peroxides and glutathione homeostasis were studied in an experimental model using re-fed rats. The animals treated with piroxicam (10-20 mg/kg) had a dose-dependent increase in the severity of intestinal lesions, but only the highest dose of meloxicam (15 mg/kg) caused macroscopic damage. The severity of piroxicam and meloxicam-induced damage was correlated with a significant increase of xantine oxidase activity and a decrease of superoxide dismutase activity and glutathione levels (P<0.05 and P<0.001 vs. control). In contrast, there was no significant neutrophil infiltration of the intestine after dosing. Our results support the hypothesis that oxygen free radicals, probably derived via the action of xantine oxidase, the decrease in superoxide dismutase activity, and depletion of mucosal glutathione contribute to the pathogenesis of meloxicam and piroxicam-induced intestinal ulceration in re-fed rats.

Topics: Animals; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Eating; Female; Food-Drug Interactions; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Intestinal Mucosa; Isoenzymes; Male; Meloxicam; Membrane Proteins; NADH, NADPH Oxidoreductases; Oxidative Stress; Piroxicam; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Wistar; Superoxide Dismutase; Thiazines; Thiazoles; Thioredoxin-Disulfide Reductase; Ulcer

Topics: Anti-Inflammatory Agents, Non-Steroidal; Clinical Trials as Topic; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Humans; Intestinal Perforation; Meloxicam; Prospective Studies; Thiazines; Thiazoles; Ulcer