gastrins and carprofen

The effects of indomethacin and carprofen on gastric secretion, serum gastrin level, electropotential difference, gastric microbleeding, DNA loss, mucosal blood flow and the production of mucosal prostaglandins (PGs) were investigated in a double-blind cross-over study in 18 healthy volunteers after one week of treatment. We did not observe any significant changes in basal and pentagastrin-stimulated gastric secretory parameters, serum gastrin level and electro-potential difference before and after treatment with these drugs. Mucosal blood flow was significantly reduced following indomethacin treatment. The most pronounced differences were found in endoscopic score studies of gastric mucosa. After indomethacin all subjects developed multiple erosions, submucosal haemorrhages, and half of them showed diffuse antral erythema. These effects were accompanied by a significant increase in both gastric microbleeding and DNA loss, and significant decrease in the production of PGE2. We concluded that carprofen, in contrast to indomethacin, did not alter gastric mucosal integrity and production of PGE2. This study indicates that the gastric mucosal damage by non-steroid anti-inflammatory compounds (NOSAC) depends upon the suppression of PGE2 biosynthesis, and that endogenous PGE2 is involved in the control of mucosal blood flow and mucosal integrity.

Topics: Adult; Anti-Inflammatory Agents; Blood Circulation; Carbazoles; Clinical Trials as Topic; Dinoprostone; Double-Blind Method; Endoscopy; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Humans; Indomethacin; Male; Prostaglandins E; Stomach

The effects of carprofen (Roche), a nonsteroid antiinflammatory agent, on gastric secretion, serum gastrin level, electropotential difference (PD), gastric microbleeding, DNA loss, and the generation of mucosal prostaglandins (PGs) were examined in 20 duodenal ulcer patients with active ulcer (15 patients) or in remission (5 patients). Carprofen administered for one-week period at a therapeutic dose (300 mg/day) was well tolerated by all ulcer patients and no adverse effects were observed during or after treatment. Endoscopy performed after carprofen treatment showed complete ulcer healing in 9 out of 15 patients and no exacerbations were observed in the rest of patients. No significant changes were observed in basal or pentagastrin-induced secretion, PD, gastric microbleeding and DNA loss. The generation of PGE2, 6-keto-PGF1 alpha and thromboxane B2 was not affected by the treatment with carprofen. This study indicates that carprofen shows excellent gastrointestinal tolerance in ulcer patients, and it might be useful in the treatment of arthritic patients with peptic ulcer disease.

Topics: Action Potentials; Adult; Anti-Inflammatory Agents; Carbazoles; DNA; Duodenal Ulcer; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Peptic Ulcer Hemorrhage; Prostaglandins