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DOI 10.1016/j.micpath.2016.09.016

Медицинская библиотека · Microbial pathogenesis · 2016

Clinical relevance of Helicobacter pylori virulence factors in Iranian patients with gastrointestinal diseases.

Bagheri Nader, Azadegan-Dehkordi Fatemeh, Rafieian-Kopaei Mahmoud, Rahimian Ghorbanali, Asadi-Samani Majid, Shirzad Hedaytollah

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Аннотация

Helicobacter pylori (H. pylori) usually colonizes the gastric mucosa of more than 50% of the human population, causing an infection that may appear in early childhood and can persist for life. H. pylori is suggested as the main cause of peptic ulcer and chronic gastritis. It is also associated with gastric cancer. Its severity and symptoms depend on environmental factors, host susceptibility and bacterial components, which allow H. pylori to switch between commensalism and pathogenicity. H. pylori is genetically highly variable, and the variability which affects H. pylori virulence factors might be useful in identifying the strains with different degrees of pathogenicity. The geographic distribution of distinct H. pylori genotypes is largely unknown and should be established. The prevalence of more pathogenic genotypes in certain areas may have important epidemiological consequences. It also might be associated with the severity of H. pylori related diseases in such regions. Given that Iran is located in the Middle East and Asian populations have revealed high levels of gastric cancer, it is of clinical interest to clarify the potential of H. pylori virulence markers in predicting the associated clinical outcomes. In this review, clinical relevance of adhesion molecules and significant virulence factors of H. pylori in Iranian patients with gastrointestinal diseases are discussed in comparison to other countries.

Для цитирования: Bagheri Nader, Azadegan-Dehkordi Fatemeh, Rafieian-Kopaei Mahmoud, Rahimian Ghorbanali, Asadi-Samani Majid, Shirzad Hedaytollah. Clinical relevance of Helicobacter pylori virulence factors in Iranian patients with gastrointestinal diseases.. Microbial pathogenesis. 2016. DOI: 10.1016/j.micpath.2016.09.016.

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