| Project/Area Number |
08671489
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Nippon Medical School |
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Principal Investigator |
MATSUKURA Norio Dept.of Surg., Nippon Medical School, Assistant Prof., 医学部, 講師 (70124427)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Peptic ulcer / Helicobacter pylori / Perforation / Cytotoxin gene / cagA / vacA / case-control study / etiology / 胃十二指腸潰瘍 / 潰瘍合併症 / 穿孔部閉鎖術 / PCR |
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| Research Abstract |
Evidence showed a marked decrease in recurrence rate of peptic ulcer following eradication of Helicobacter pylori infection. However, whether H.pylori infection is etiologically related to perforation of peptic ulcer remains to be clarified. We therefore conducted and age and gender matched case-control study between perforated and non-surgical peptic ulcers in H.pylori infection and examined differences in cytotoxin genes, cag A and vac A.Serum H.pylori IgG antibody (ELISA) was positive in 20/21 (95%) of perforated vs. 37/40 (93%) of non-surgical duodenal ulcer and 5/5 (100%) of perforated vs. 24/28 (86%) of non-surgical gastric ulcer patients. Positivity of H.pylori DNA in gastric juice, which was amplified by PCR and identified by Southern blot hybridization was 17/23 (74%) of perforated vs. 32/45 (71%) in the non-surgical duodenal ulcer group. Positivity of cytotoxin genes, cagA and vacA ; in H.pylori DNA-positive gastric juice was as follows : perforated vs. non-surgical duodenal ulcer, cagA : 11/13 (85%) vs. 24/27 (89%) ; vacA1 : 9/13 (69%) vs. 22/27 (82%) ; vacA2 8/13(62%) vs. 21/27 (78%). There was no significant differences between the perforated and non-surgical peptic ulcers groups for these H.pylori serum and gene markers. It is assumed that H.pylori infection is not etiologically related to perforation of peptic ulcer.
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