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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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Guidelines in the medical treatment of Helicobacter pylori infection

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Scientific evidence based on controlled clinical research confirm substantial benefits resulting from the eradication of H. pylori infection in such pathologies of the alimentary tract as: gastric peptic and duodenal ulcer (active or confirmed in the future and ulcer disease complications), MALT (Mucosa Associated Limphoid Tissue) lymphoma, atrophic gastritis, past stomach resection, gastric cancer in the family. The above group of indications is strongly recommended for eradicative treatment. During the last several years there have been many guidelines made by international and national specialist groups. “Test and treat” strategy of undiagnosed dyspepsia treatment is based on possibility to carry out non-invasive tests confirming H. pylori infection. First symptoms of dyspepsia in people over 45 years of age constitute recommendation for endoscopy, as well as symptoms assumed to be “alarming” (loss of weight, anaemia, bloody vomiting, tarry stool, dysphagia) regardless of patient age. An individual approach to eradication is proposed in gastroesophageal reflux disease, and use of non-steroid anti-inflammatory drugs. Antibacterial activity towards H. pylori is shown by many antibiotics (amoxicillin, macrolides, tetracyclines) and some other chemotherapeutic agents (nitroimidazoles) and bismuth. PPIs are recommended, because through increase of pH in stomach they create conditions to act for antibiotics. During the stage of first line triple therapy, it is advised to apply PPI and two antibacterial medicines at the same time (PPI + amoxicillin+metronidazole or clarithromycin). Such therapeutic action ensures achievement of eradication of H. pylori infection in 80-90% of cases. In case of lack of treatment efficiency in the first-line therapy, 7-14 day treatment may be repeated using triple therapies (PPI + 2 antibiotics) substituting the antibiotic with the metronidazole or tetracycline, or quadruple therapies (PPI + bismuth citrate + 2 antibiotics). Side effects during eradicative treatments occur quite rarely (from 15 to 30%).
Helicobacter pylori (H. pylori) is an important gastrointestinal pathogen associated with gastritis as well as gastric or duodenal ulcers and gastric cancer. The oral cavity has been considered as a potential reservoir for the gastric infection and reinfection. The objective of our studies was to evaluate the influence of oral H. pylori for the stomach infection and the release of gut hormones affecting food intake such as ghrelin and gastric secretion such as gastrin. Additionally, the contribution of H. pylori in the periodontal disease has been examined. H. pylori infection in stomach was assessed by 13C- Urease Breath Test and presence of the bacteria in oral cavity by culture. The periodontal status was measured by pockets depth with the periodontal probe. We estimated the serum level of IgG anti-H. pylori, anti-VacA, anti-CagA, ghrelin, gastrin, TNF-alpha and IL-8 in blood and the level of IgA anti-H. pylori in saliva. The presence of H. pylori in oral cavity was detected in 54.1% of examined individuals, whereas the H. pylori gastric infection in tested group was found in 51% cases. However, the correlation analysis between those two groups of patients involving together about 100 subjects showed that within the group of patients with positive gastric H. pylori infection only 45.1% did not show the presence of H. pylori in saliva and 43.1% showed no H. pylori in supragingival plaque. In line of these findings patients who did not have gastric H. pylori infection, 53.2 % showed presence of H. pylori in saliva and 42.9% in supragingival plaques. Serum level of ghrelin and gastrin in subjects with oral H. pylori inoculation but without gastric H. pylori infection were not significantly different from those without the presence of this germ in oral cavity. In contrast, gastric H. pylori infection resulted in significant reduction in serum ghrelin levels and significant elevation of gastrin as compared to those who were gastric H. pylori negative. We concluded that oral H. pylori alone does not seem to serve as bacterium sanctuary for gastric H. pylori infection and, unlike gastric infection, it fails to affect serum levels of hormones stimulating appetitive behaviour such as ghrelin and gastric acid secretion such as gastrin.
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