PMID- 19219527 OWN - NLM STAT- MEDLINE DCOM- 20090402 LR - 20211020 IS - 1661-4917 (Electronic) IS - 0004-069X (Print) IS - 0004-069X (Linking) VI - 57 IP - 1 DP - 2009 Jan-Feb TI - Virulence factor genotypes of Helicobacter pylori affect cure rates of eradication therapy. PG - 45-56 LID - 10.1007/s00005-009-0007-z [doi] AB - 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. FAU - Sugimoto, Mitsushige AU - Sugimoto M AD - Department of Medicine, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, TX, USA. FAU - Yamaoka, Yoshio AU - Yamaoka Y LA - eng GR - R01 DK062813/DK/NIDDK NIH HHS/United States GR - R01 DK062813-05/DK/NIDDK NIH HHS/United States GR - R01 DK62813/DK/NIDDK NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Review DEP - 20090214 PL - Poland TA - Arch Immunol Ther Exp (Warsz) JT - Archivum immunologiae et therapiae experimentalis JID - 0114365 RN - 0 (Anti-Bacterial Agents) RN - 0 (Anti-Ulcer Agents) RN - 0 (Antigens, Bacterial) RN - 0 (Bacterial Proteins) RN - 0 (Cytokines) RN - 0 (Histamine H2 Antagonists) RN - 0 (VacA protein, Helicobacter pylori) RN - 0 (cagA protein, Helicobacter pylori) SB - IM MH - Anti-Bacterial Agents/administration & dosage/pharmacokinetics/therapeutic use MH - Anti-Ulcer Agents/administration & dosage/therapeutic use MH - Antigens, Bacterial/genetics/physiology MH - Bacterial Proteins/genetics/physiology MH - Cytokines/biosynthesis/genetics MH - Drug Resistance, Multiple, Bacterial MH - Drug Therapy, Combination MH - Gastric Acid/metabolism MH - Gastritis/complications/drug therapy/*microbiology MH - Genomic Islands/genetics MH - Genotype MH - Helicobacter Infections/complications/drug therapy/*microbiology MH - Helicobacter pylori/drug effects/genetics/isolation & purification/*pathogenicity MH - Histamine H2 Antagonists/administration & dosage/therapeutic use MH - Host-Pathogen Interactions MH - Humans MH - Remission Induction MH - Stomach Neoplasms/etiology/microbiology MH - Stomach Ulcer/etiology/microbiology MH - Virulence/genetics PMC - PMC3118989 MID - NIHMS178139 COIS- Disclosure: No conflicts of interest exist in this manuscript. EDAT- 2009/02/17 09:00 MHDA- 2009/04/03 09:00 PMCR- 2011/06/21 CRDT- 2009/02/17 09:00 PHST- 2008/07/07 00:00 [received] PHST- 2008/10/20 00:00 [accepted] PHST- 2009/02/17 09:00 [entrez] PHST- 2009/02/17 09:00 [pubmed] PHST- 2009/04/03 09:00 [medline] PHST- 2011/06/21 00:00 [pmc-release] AID - 10.1007/s00005-009-0007-z [doi] PST - ppublish SO - Arch Immunol Ther Exp (Warsz). 2009 Jan-Feb;57(1):45-56. doi: 10.1007/s00005-009-0007-z. Epub 2009 Feb 14.