Homeostasis between indigenous intestinal flora and host response may be broken in inflammatory bowel disease. The present study explores whether repeated oral administration of intestinal flora antigens can protect mice against dextran sodium sulphate (DSS)‐induced colitis. Sonicates of Gram‐positive, Gram‐negative, or anaerobic resident bacteria isolated from mouse intestinal flora were fed to BALB/c mice by gastric gavage, with or without cholera toxin. After four weekly doses of 1 mg of these antigen preparations (or of PBS as control), DSS colitis was induced. One week later colitis was evaluated by clinical scores and histology. Mice fed a pool of the three sonicates had decreased inflammation scores (5 (1–14); median (range)) compared with PBS‐fed control animals (15 (7–19); P < 0·05). Decreased inflammation was observed in mice fed anaerobic bacteria antigens (7 (6–11); P < 0·05 versus control), but not in mice fed a pool of Gram‐positive and ‐negative sonicates (16 (12–16)). Inflammation scores of mice fed antigens with cholera toxin were similar to those of PBS‐fed control animals. DSS‐induced colitis can be suppressed by oral administration of normal intestinal flora antigens containing anaerobes.
Compared to Ultraflex stents, Wallstents have several significant short-term and long-term advantages in the palliative treatment of malignancy of the esophagus and cardia.
Since their introduction in 1976, and until recently, the H2-receptor antagonists have been the ‘state-of-the-art’ gastric acid inhibitors, but the advent of omeprazole, the acid pump inhibitor, has necessitated a reassessment of therapy for acid-related diseases. In making this reassessment, the following therapeutic goals should be considered: rapid and reliable therapeutic effect, safety, simple treatment regimen, resolution of recurrence, and cost-effectiveness. Extensive clinical evidence indicates that omeprazole offers an advance over the H2-receptor antagonists in achieving these goals. A series of meta-analyses shows that omeprazole gives more rapid symptom relief and more reliable healing than the H2-receptor antagonist, ranitidine, in uncomplicated duodenal ulcer (DU), in uncomplicated gastric ulcer (GU) and in reflux oesophagitis (RO). By contrast with the H2-receptor antagonists, refractoriness leading to failure to heal is virtually unknown with omeprazole. Omeprazole also fulfils the goal of therapeutic safety, and this has been documented in extensive short- and long-term clinical and laboratory studies. Omeprazole has a simple treatment regimen: 20 mg once daily is recommended in the routine treatment of DU, GU and RO. As a result of its high therapeutic success rate, omeprazole is also cost-effective. Taking all these factors into account, it is concluded that omeprazole approaches the therapeutic targets set for the treatment of acid-related disorders.
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