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In this article, we evaluate whether currently available evidence supports the existence of factors important in the development of duodenal ulcer disease.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods.<\/jats:title><jats:p>The evaluation is conducted by a review of the literature on<jats:italic>H. pylori<\/jats:italic>toxins and virulence factors.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results.<\/jats:title><jats:p>Most putative<jats:italic>H. pylori<\/jats:italic>virulence factors are present in all isolates examined, though some are present only in, or are expressed more intensively by, determined strains. Urease is the main virulence determinant of<jats:italic>H. pylori<\/jats:italic>. It generates ammonia from the gastric urea, which in turn injures the gastric mucosa either directly by forming ammonium hydroxide or indirectly by stimulating polymorphonuclear leukocytes and inhibiting cell proliferation. Other enzymes (e.g., mucinase, phospholipases, alcohol dehydrogenase, neuraminidase) could promote tissue erosion and ulceration by destroying the integrity of mucus, by inducing lipid peroxidation, and the like.<\/jats:p><jats:p><jats:italic>H. pylori<\/jats:italic>strains that express the vacuolating toxin<jats:italic>vac<\/jats:italic>A and the associated protein<jats:italic>cag<\/jats:italic>A are called<jats:italic>type I<\/jats:italic>and are considered to be endowed with increased ulcerogenic and inflammatory potential. Exploration of the structure of the<jats:italic>vac<\/jats:italic>A gene has shown that the degree of toxicity is regulated at the molecular level. Type I<jats:italic>H. pylori<\/jats:italic>strains carry a 40\u2010kb genomic fragment called<jats:italic>cag<\/jats:italic>that is absent from type II strains (<jats:italic>vac<\/jats:italic>A\u2010 and<jats:italic>cag<\/jats:italic>A\u2010negative).<jats:italic>cag<\/jats:italic>is considered a pathogenicity island because it contains numerous genes that are highly homologous to virulence genes of classic bacterial pathogens and because it has been suggested that it is acquired through recombination events.<jats:italic>CagA<\/jats:italic>is part of the pathogenicity island.<jats:italic>Cag<\/jats:italic>A\u2010positive strains are more likely to be isolated from patients with duodenal ulcer and other severe digestive pathological processes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions.<\/jats:title><jats:p>The use of simple serological tests to identify patients infected with type I<jats:italic>H. pylori<\/jats:italic>strains could help to calculate the risk of development of severe gastroduodenal diseases and, possibly, to prevent such severe diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1523-5378.1997.06b06.x","type":"journal-article","created":{"date-parts":[[2007,6,27]],"date-time":"2007-06-27T14:42:26Z","timestamp":1182955346000},"page":"3-12","source":"Crossref","is-referenced-by-count":17,"title":["Identifiable<i>Helicobacter pylori<\/i>Strains or Factors Important in the Development of Duodenal Ulcer Disease"],"prefix":"10.1111","volume":"2","author":[{"given":"Natale","family":"Figura","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2007,6,27]]},"reference":[{"key":"e_1_2_8_2_2","unstructured":"Helicobactergenus: The history ofH. pyloriand taxonomy of current species. 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