2005 Fiscal Year Final Research Report Summary
Formulating a method of determining the efficacy of H.pylori eradication with pulsed field gel electrophoresis
Project/Area Number |
15590497
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Laboratory medicine
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Research Institution | Showa University |
Principal Investigator |
CHEN Gelin Showa University, School of Medicine, Research assistant, 医学部, 助手 (60266111)
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Co-Investigator(Kenkyū-buntansha) |
FUKUCHI Kunihiko Showa University, School of Medicine, Associate Professor, 医学部, 助教授 (70181287)
TAKAGI Asushi Showa University, School of Medicine, Professor, 医学部, 教授 (30138490)
GOMI Kunihide Showa University, School of Medicine, Professor, 医学部, 教授 (60053980)
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Project Period (FY) |
2003 – 2005
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Keywords | Helicobacter pylori / pulsed-field gel electrophoresis / genotyping / eradication treatment / drug resistance / PCR / cagA |
Research Abstract |
With a molecular technique, we attempted to determine the efficacy of Helicobacter pylori eradication, study changes in the rate of infection, and study the prevalence of cagA, a virulence factor for H.pylori. In the first year of the study, we compared H.pylori's pattern of sensitivity to the three agents of AMPC, CAM, and MNZ detected before and after eradication in a total of 28 specimens from before and 2-3 months after treatment in 14 cases in which eradication was performed with the three agents of LPZ+AMPC+CAM from January 2001-January 2002. We also studied the causes of eradication failure through genomic analysis with pulsed field gel electrophoresis (PFGE). In 5 cases where eradication failed, the genotypes before and after treatment matched. Three cases were sensitive to all 3 agents before and after eradication ; the remaining 2 cases had primary resistance to CAM before treatment. These cases cannot be considered to have acquired resistance due to eradication, so the cause
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of failed eradication was not development of resistance or re-infection but was because the eradication agents were not taken correctly. In the second year of the study, we examined changes in the rate of H.pylori infection using an HpSA ELISA reagent for fecal antigen detection and the state of infection of clinical technicians routinely handling H.pylori. With regard to the rate of infection, there was only a shift in positive rates for individual age groups in comparison to 10 years prior. Of 7 technicians routinely handling H.pylori, 2 were positive for H.pylori fecal antigens. In contrast to a report of a rate of H.pylori infection of 50% or more in health care personnel such as endoscopists, this phenomenon was not noted in bacteriology technicians involved in H.pylori testing. In the third year, we examined cagA, a virulence factor for H.pylori, with PCR. One hundred and six of 108 clinically isolates possessed cagA ; this agreed with a report of 95-100% of clinically isolates possessing cagA. This suggests that possession of cagA may not serve as an indicator for onset by H.pylori or prognosis. Less
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Research Products
(2 results)