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The presence of spiral-shaped micro-organisms in the human stomach was described over 100 years ago by Polish clinical researcher, Professor W. Jaworski at Cracow Jagiellonian University. Their presence was then confirmed in animals by G. Bizzazero, but was not really taken seriously until the late 1970s, when J.R. Warren, a pathologist in Perth, Australia, noted the appearance of spiral bacteria overlaying gastric mucosa, chiefly over inflamed tissue. Warren and B.J. Marshall cultured these organisms in 1982 from 11 patients with gastritis and were able to demonstrate a strong association between the presence of Helicobacter pylori (H. pylori) and the finding of inflammation in gastric biopsies. People, who did not exhibit gastritis, also did not have the organism, a finding which was confirmed in a number of studies. Originally called Campylobacter pyloridis, the name was changed to Campylobacter pylori, and then later to Helicobacter pylori (H. pylori) as specific morphologic, structural, and genetic features indicated that it should be placed in a new genus. Marshall elegantly fulfilled Koch's postulates for the role of H. pylori in antral gastritis with the self administration of H. pylori, and also showed that it could be cured by use of antibiotics and bismuth salts. Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. The role of H. pylori in non-ulcer dyspepsia remains unclear. These practical aspects of H. pylori were subjects of two international symposia organized by us in 1995 and 1997 in Cracow, helping to promote research and Polish consensus regarding treatment of H. pylori infection.
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Prostaglandins and ulcer healing

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Exogenous prostaglandins (PG) applied in small gastroprotective doses fail to affect healing of gastro-duodenal ulcers but accelerate the healing when used in larger gastric inhibitory doses that appear to enhance COX-2 expression and PGE2 generation in the ulcer area. COX-1 and COX-inhibitors delay ulcer healing, particularly when both COX isoforms are suppressed such e.g. by indomethacin. Dexamethasone, that decreases the expression of COX-2 and mucosal generation of PGE2, delays ulcer healing that can be reversed by the addition of small dose of exogenous PGE2. Proton pump inhibitors (PPI) such as omeprazole and PGE analogs, accelerate ulcer healing mainly due to potent inhibition of gastric acid secretion, but they also augment the COX-2 expression and enzyme activity in the ulcerated mucosa. Endogenous PG generated at ulcer margin appear to be involved in ulcer healing promoted by growth factors and gut hormones such as gastrin or CCK and melatonin acting, at least in part, through increase of induction of COX-2 and local release of PGE2 in the ulcer area . The ulcer healing activity of growth factors (e.g. EGF, TGFalpha, HGF) and certain gut hormones (gastrin, CCK) as well as melatonin, can be attenuated by treatment with COX-1 or COX-2 inhibitors which suppress the release of PGE2 but enhance the expression of COX-2. It is concluded that endogenous PG originating mainly from upregulated COX-2 at the ulcer margin play crucial role in ulcer healing by exogenous PG, PPI, growth factors, gut hormones and melatonin, while COX-1 and COX-2 inhibitors delay ulcer healing by suppressing PG generation, and increasing COX-2 expression in the ulcer area.
The discovery of Helicobacter pylori (H. pylori) provided a possibility to cure effectively patients with peptic ulcers. Recent studies have shown varying susceptibility of H. pylori strains to antibiotics and increasing resistance to some of the recommended drugs. The purpose of the present study was to evaluate the efficacy of the currently recommended eradication schemes and to assess the increasing resistance of H. pylori strains to recommended antibiotics. Furthermore, the effect of probiotics (Lacidofil) on the efficacy of first-line treatment with amoxicillin and clarithromycin was analyzed. The study population consisted of 641 patients: 192 received amoxicillin with clarithromycin and proton pump inhibitor (PPI), 241 - tetracycline, tinidazole, bismuth and PPI, 53 - amoxicillin with clarithromycin and PPI supplemented with Lacidofil. The efficacy of eradication treatment was evaluated by the 13C-urease breath test. The microbiological examination included 111 samples of H. pylori. The present study demonstrated low efficacy of the tetracycline, tinidazole, bismuth and PPI scheme i.e. 71.4%, moderate efficacy of the amoxicillin with clarithromycin and PPI scheme i.e. 85.9%, whereas the supplementation with Lacidofil significantly increased the efficacy of eradication to 94.3%. The microbiological examination revealed a relatively high level of primary resistance to clarithromycin (22.2%) and a high level to metronidazole (46.7%), with no resistance to amoxicillin. However, the most important finding is the high level of secondary resistance to clarithromycin and metronidazole (more than 66% in both cases). The present findings suggest the need for modification of the recommended eradication schemes.
Solcoseryl, a deproteinized extract of calf blood, protects the gastric mucosa against various topical irritants and enhances the healing of chronic gastric ulcerations but the mechanisms of these effects have been little studied. This study was designed to elucidate the active principle in Solcoseryl and to determine the role of prostaglandisn (PG) and polyamines in the antiulcer properties of this agent. Using both, the radioimmunoassay and radioreceptor assay, EGF-like material was detected in Solcoseryl preparation. Solcoseryl given s. c. prevented the formation of stress-indused gastric lesions and this was accompanied by an increase in the generation of PGE2 in the gastric mucosa. Similar effects were obtained with EGF. Pre treatment with indomethacin, to suppress mucosal generation of prostaglandins (PG), greatly augmented stress- induced gastric ulcerations and antagonized the protection exerted by both Solcoseryl and EGF. Solcoseryl, like EGF, enhanced the healing of chronic gastroduodenal ulcerations. This effect was abolished by the pretreatment with difluoro- methylomithine, an inhibitor of ornithine decarboxylas, the key enzyme in the biosynthesis of polyamines. The healing effects of Solcoseryl and EGF was also reduced by prednisolone which decreased the angiogenesis in the granulation tissue in the ulcer area. These results indicate that Solcoseryl 1. contains EGF-like material, 2. displays the protective and ulcer healing effects similar to those of EGF and involving both PG and polyamines and 3. acts via similar mechanism as does EGF.
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