Over the last 25 years, a remarkable revolution in the pathophysiology and treatment of gastric and duodenal ulcers has occurred. Effective therapies were developed not only to heal ulcers, but also to cure most patients. The two principal causes for gastric and duodenal ulcers are either infection with Helicobacter pylori or the use of non-steroidal anti-inflammatory drugs (NSAIDs). With H. pylori eradication, gastric and duodenal ulcers are rapidly becoming historical diseases. This communication reviews the salient pharmacology of the novel anti-ulcer drugs currently in development, with particular emphasis on the treatment of gastric and duodenal ulcers. Intense research is currently focused on the development of proton pump inhibitors primarily for the treatment and prevention of gastroesophageal reflux disease. The older proton pump inhibitors, omeprazole and lansoprazole, are effective in healing gastric and duodenal ulcers. Furthermore, both drugs are effective in eradicating H. pylori when given with various antibiotics. Pantoprazole, rabeprazole and esomeprazole are new proton pump inhibitors, which appear to have comparable therapeutic profiles with omeprazole and lansoprazole. Rebamipide is a new mucosal protective drug, which is effective in healing gastric ulcers. Polaprezinc and nocloprost are also mucosal protective drugs, which are in clinical development. However, none of these three cytoprotective drugs have been evaluated for their efficacy in eradicating H. pylori when given in combination with antibiotics. Likewise, no published literature exists on the use of these drugs for preventing NSAID-induced ulcers. With the rapid eradication of H. pylori currently happening in the developed world, the therapeutic challenge is now directed toward preventing NSAID-associated ulcer. Significant reduction of NSAID-induced ulcers is achieved by using continuous prophylactic anti-ulcer therapy (misoprostol or omeprazole) or by using NSAIDs possessing selective COX-2 inhibitory activity. However, outcome clinical studies are needed to compare the adjuvant anti-ulcer therapies given with COX-1 inhibitors versus the selective COX-2 inhibitors given alone.

01 Jul 1998·Prostaglandins, Leukotrienes and Essential Fatty AcidsQ3 · MEDICINE

Effects of PGE2 and of different synthetic PGE derivatives on the glycosylation of pig gastric mucins

Q3 · MEDICINE

Article

Author: Eisenblatter, R. ; Enss, M.-L. ; Heim, H.-K. ; Beil, W. ; Sewing, K.-F. ; Wagner, S. ; Hedrich, H. J.

The glycosylation of pig gastric mucins, discharged in response to prostaglandin (PG) E2 and to three synthetic PGE-derivatives (misoprostol, nocloprost, rioprostil) was compared. After a 20 h culture period in the absence or presence of 1 micromol/l of one of the PGs, mucins were isolated by gel chromatography and their glycosylation characterized by their linkage to a panel of lectins. For all tested PGs, a significantly increased lectin linkage to mucin glycoproteins of high molecular weight was detected; no significant effects were observed for low molecular weight glycoproteins. Within the stimulatory pattern, major effects were found for the linkage of peanut agglutinin and soybean agglutinin, suggesting predominant effects on the expression of galactose and N-acetyl-galactosamine. Only minor effects were found for sialic acid, mannose, N-acetyl-glucosamine and fucose expression, as evidenced by the linkage of Sambucus nigra agglutinin, Concanavalin A, Datura stramonium agglutinin and Ulex europaeus I agglutinin. All PGs exerted a similar stimulatory pattern. However, at the indicated concentration, misoprostol (281 +/- 36% of control) rendered a significantly higher overall effect than PGE2 (208 +/- 31%), whereas the increases induced by nocloprost (237 +/- 35%) and rioprostil (202 +/- 35%) were not significantly different from the PGE2 effects. These results, suggesting similar stimulatory effects of PGE2 and of the tested synthetic PGs on glycosylation of mucin oligosaccharides, discharged from mucous cells during an in vitro culture, may, at least in part, explain clinical findings that during an impairment of the endogenous PG synthesis, the tested synthetic PGs are effective exogenous substitutes for endogenous E-type prostaglandins and act as anti-ulcer drugs.

01 Jan 1997·Roczniki Akademii Medycznej w Bialymstoku (1995)

Effects of ranitidine or nocloprost on the selected gastric juice components in the patients with the gastric ulcer.

Article

Author: Gabryelewicz, A ; Skrodzka, D

The 24 patients with gastric ulcer were treated ranitidine (2 x 150 mg daily) or nocloprost (2 x 200 micrograms daily). The effects of these drugs on the gastric juice components were measured. We evaluated hydrochloric acid, total protein, pepsin and some carbohydrates components secretion. We showed, that ranitidine decreased significantly total protein, fucose, N-acetylneuraminic acid and hexoses contents in the gastric juice in the basal secretion; the same tendency was observed in the pentagastrin-stimulated secretion. The similar direction of the changes, but weakly expressed was confirmed in the patients treated with nocloprost. It has been shown, that ranitidine modified the gastric mucin components content, what can suggest diminished degradation of mucus directly adhering to the gastric mucosa.

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Indication	Highest Phase	Country/Location	Organization	Date
Peptic Ulcer	Phase 3	-	Bayer AG	-
Peptic Ulcer	Phase 3	-	Bayer AG	-

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