title: Virulence factor genotypes of Helicobacter pylori affect cure rates of eradication therapy.
abstract: The cure rates of Helicobacter pylori infection by using a combination of a proton pump inhibitor (PPI) and antimicrobial agents are mainly influenced by bacterial susceptibility to antimicrobial agents and the magnitude of acid inhibition during the treatment. Currently used empirical triple therapies do not reliably produce a > or =80% cure rate on an intention-to-treat basis. Therefore, tailored regimens based on relevant microbiological findings and pharmacogenomics are recommended for attaining an acceptable > or =95% cure rate. Recently, virulence factors of H. pylori, such as cagA and vacA, are reported to be major factors determining the cure rates. Individuals infected with strains with cagA-negative and vacA s2 genotypes have significantly increased risk of eradication failure of H. pylori infection. These virulence factors enhance gastric mucosal inflammation and are associated with the development of peptic ulcer and gastric cancer. H. pylori virulence factors induce proinflammatory cytokines, such as interleukin (IL)-1, IL-8, and tumor necrosis factor (TNF)- which influence mucosal inflammation and/or gastric acid secretion. When physicians select an H. pylori eradication regimen with an acceptable cure rate, they might need to consider H. pylori virulence factors, especially cagA and vacA.
authors.affiliation: Department of Medicine, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, TX, USA.
authors.forename: Mitsushige
authors.initials: M
authors.lastname: Sugimoto
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Yamaoka
mesh_terms: D000900:Anti-Bacterial Agents / Q000008:administration & dosage / Q000493:pharmacokinetics / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000008:administration & dosage / Q000627:therapeutic use; D000942:Antigens, Bacterial / Q000235:genetics / Q000502:physiology; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D024901:Drug Resistance, Multiple, Bacterial; D004359:Drug Therapy, Combination; D005744:Gastric Acid / Q000378:metabolism; D005756:Gastritis / Q000150:complications / Q000188:drug therapy / Q000382:microbiology*; D044404:Genomic Islands / Q000235:genetics; D005838:Genotype; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy / Q000382:microbiology*; D016480:Helicobacter pylori / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D006635:Histamine H2 Antagonists / Q000008:administration & dosage / Q000627:therapeutic use; D054884:Host-Pathogen Interactions; D006801:Humans; D012074:Remission Induction; D013274:Stomach Neoplasms / Q000209:etiology / Q000382:microbiology; D013276:Stomach Ulcer / Q000209:etiology / Q000382:microbiology; D014774:Virulence / Q000235:genetics
chemical_list: D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D016207:Cytokines; D006635:Histamine H2 Antagonists; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori