misoprostol and Stomach-Neoplasms

An endoscopic screening was carried out during the period between July 1989 and December 1991 in the Municipality of Roccagorga (LT) in order to: a) evaluate the presence of various forms of gastritis and pre-cancerous lesions; 2) verify the effect of the administration of prostaglandins (Misoprostol) on the evolution of superficial chronic gastritis (CG). A total of 468 endoscopy were performed (17% of the population aged between 20 and 75 years old). 22% of the subjects examined were found to be endoscopically normal; 34% presented symptoms of mild esophagitis and 4% of moderate esophagitis. The prevalence of duodenal ulcer was 10.6% and gastric ulcer 3.4%. Gastric carcinoma was diagnosed in 6 patients (1.2%). 8.5% of patients were found to have atrophic CG and 15.3% superficial CG. Thirty-six patients with superficial CG were randomly divided into two groups: A) treated with Misoprostol 600 mg/day for 6 months; B) controls (placebo). The administration of Misoprostol did not influence the evolution of CG, whereas it caused a reduction in the incidence of type 1 intestinal metaplasia. Misoprostol also led to an improvement in dyspeptic symptoms. The results of the present study do not suggest a role of prostaglandins in the natural evolution of CG.

Topics: Adult; Aged; Chronic Disease; Diagnosis, Differential; Duodenal Ulcer; Female; Gastritis; Gastroscopy; Humans; Male; Middle Aged; Misoprostol; Stomach Neoplasms; Stomach Ulcer

The purpose of this study was to investigate the effect of long-term misoprostol administration, at non-antisecretory doses, on N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)-induced gastric carcinogenesis. The incidence of gastric carcinomas and precancerous lesions was evaluated in 50 male 250-g Sprague-Dawley rats after 52 weeks of continuous oral administration of MNNG (120 mg/l; n = 20), MNNG plus misoprostol (2 mg kg-1 day-1; n = 20) or tap water (n = 10) (experiment 1), and in 30 rats treated with MNNG for 30 weeks followed by tap water (n = 15) or by misoprostol (n = 15) for 22 weeks; a third group (n = 10) received tap water only for 52 weeks (experiment 2). After sacrifice, gastric mucosal lesions were macroscopically evaluated and their histology obtained. MNNG consumption was comparable in all groups (6.5 +/- 1.1 mg rat-1 day-1). Misoprostol consumption was 180 +/- 0.25 mg kg-1 day-1 rat-1. In experiment 1 the incidence of gastric carcinomas was 60% in the MNNG group and 25% in the group treated with MNNG plus misoprostol (P less than 0.05). Cytotoxic and hyperplastic gastric mucosal lesions were also significantly reduced by misoprostol. In experiment 2 the incidence of carcinomas was 31% and 38.6% respectively. Misoprostol significantly decreased the incidence of gastric cancer formation when given from the beginning of the experiment. By contrast, when administered after 30 weeks of MNNG treatment it did not interfere with experimental gastric cancer formation. Exogenous prostaglandins are able to prevent the early MNNG-induced gastric mucosal lesions, thus interfering with gastric carcinogenesis.

Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Cell Nucleus; Cystadenocarcinoma; Male; Methylnitronitrosoguanidine; Misoprostol; Rats; Rats, Inbred Strains; Stomach Neoplasms; Time Factors