Abstract
The eradication rates of Helicobacter pylori by the triple therapy consisting of a proton pump inhibitor (PPI) and two antimicrobial agents are mainly influenced by bacterial susceptibility to antimicrobial agents and magnitude of acid inhibition during the treatment with a PPI. Acid inhibition during the treatment is affected by the dosing schemes of acid inhibitory drugs (i.e., PPI), genotypes of drug-metabolizing enzymes (i.e., CYP450 2C19), drug transporters (i.e., multi-drug resistant transporter-1) and inflammatory cytokines (i.e., IL-1 beta). Modification of dosing schedules of a PPI, such as frequent PPI dosing and concomitant dosing with a histamine 2-receptor antagonist, could overcome these genetics-related differences in therapeutic effectiveness. For attaining higher eradication rates, the tailored regimen based on the relevant pharmacogenomics is preferable.
MeSH terms
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ATP Binding Cassette Transporter, Subfamily B
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ATP Binding Cassette Transporter, Subfamily B, Member 1 / genetics
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Anti-Bacterial Agents / therapeutic use*
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Anti-Ulcer Agents / therapeutic use
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Aryl Hydrocarbon Hydroxylases / genetics
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Cytochrome P-450 CYP2C19
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Cytokines / genetics
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Drug Resistance, Bacterial
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Gastric Acid / metabolism
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Helicobacter Infections / drug therapy*
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Helicobacter Infections / genetics*
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Helicobacter Infections / metabolism
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Helicobacter pylori*
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Humans
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Mixed Function Oxygenases / genetics
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Pharmacogenetics
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Polymorphism, Genetic
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Proton Pump Inhibitors*
Substances
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ABCB1 protein, human
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ATP Binding Cassette Transporter, Subfamily B
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ATP Binding Cassette Transporter, Subfamily B, Member 1
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Anti-Bacterial Agents
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Anti-Ulcer Agents
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Cytokines
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Proton Pump Inhibitors
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Mixed Function Oxygenases
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Aryl Hydrocarbon Hydroxylases
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CYP2C19 protein, human
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Cytochrome P-450 CYP2C19