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Influence of inflammatory cytokine polymorphisms on eradication rates of <i>Helicobacter pylori</i>
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Description
<jats:title>Abstract</jats:title><jats:p>Pro‐inflammatory cytokines and anti‐inflammatory cytokines are produced in gastric mucosa from inflammatory cells activated by <jats:italic>Helicobacter pylori (H. pylori)</jats:italic> infection. Of the inflammatory cytokines, interleukin (IL)‐1β and tumor necrosis factor (TNF)‐α have a potent inhibitive effect on gastric acid production. Polymorphisms in these genes are associated with individual differences in cytokine messenger RNA levels, which result in different gastric mucosal inflammation, different acid inhibition and different gastroduodenal disease risks in response to <jats:italic>H. pylori</jats:italic> infection. The sustained higher intragastric pH during an eradication therapy is known to be one of the therapeutic determinants of the <jats:italic>H. pylori</jats:italic> eradication as well as antibiotics resistance and poor compliance. The <jats:italic>IL‐1B‐</jats:italic>511 polymorphism is related to eradication rate, and, in combined analysis of previous reports, the eradication rate in patients with the <jats:italic>IL‐1B‐</jats:italic>511 C/C genotype (77.4%, 209/270), low IL‐1β producer genotype, is lower than that of the <jats:italic>IL‐1B‐</jats:italic>511 C/T and T/T genotypes (87.2%, 631/724) (Odds ratio for eradication failure: 1.98, 95% confidence interval: 1.38–2.84, <jats:italic>P</jats:italic> = 0.0002). Moreover, the odds ratio of combined CYP2C19 rapid metabolizer‐<jats:italic>IL‐1B‐</jats:italic>511 C/C type for eradication failure is 11.15 (5.23–23.78) times that of the CYP2C19 poor metabolizer‐<jats:italic>IL‐1B‐</jats:italic>511 non‐C/C type. However, there is no positive data indicating the role of other inflammatory cytokine polymorphisms (e.g. <jats:italic>IL‐1RN</jats:italic>, <jats:italic>TNF‐A</jats:italic> or <jats:italic>IL‐10</jats:italic>) in eradication therapy. Nevertheless, the studies show that inflammatory cytokine polymorphisms, especially the <jats:italic>IL‐1B‐</jats:italic>511 T/T genotype, are the determinants of eradication by affecting gastric acid secretion and mucosal inflammation. Therefore, the tailored eradication therapy, considering inflammatory cytokine polymorphisms, may be effective for the higher eradication rates.</jats:p>
Journal
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- Journal of Gastroenterology and Hepatology
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Journal of Gastroenterology and Hepatology 24 (11), 1725-1732, 2009-10-27
Wiley
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Keywords
- Genotype
- Interleukin-1beta
- Risk Assessment
- Helicobacter Infections
- Gastric Acid
- Risk Factors
- Drug Resistance, Bacterial
- Odds Ratio
- Humans
- Polymorphism, Genetic
- Helicobacter pylori
- Tumor Necrosis Factor-alpha
- Proton Pump Inhibitors
- Anti-Bacterial Agents
- Cytochrome P-450 CYP2C19
- Phenotype
- Treatment Outcome
- Gastric Mucosa
- Cytokines
- Drug Therapy, Combination
- Aryl Hydrocarbon Hydroxylases
- Inflammation Mediators
Details 詳細情報について
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- CRID
- 1362262945283918208
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- ISSN
- 14401746
- 08159319
- 00165085
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- PubMed
- 20136959
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- Data Source
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- Crossref
- OpenAIRE