1995 Fiscal Year Final Research Report Summary
Clinical study for the pathogenesis of idiopathic chronic pancreatitis.
| Project/Area Number |
06670514
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Tohoku University |
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Principal Investigator |
KOIZUMI Masaru Tohoku Univ., School of Medicine, Lecturer, 医学部, 講師 (40111281)
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| Co-Investigator(Kenkyū-buntansha) |
MORIIZUMI S Tohoku Univ., School of Medicine, Assistant Professor, 医学部附属病院, 医員
納谷 耕司 東北大学, 医学部, 助手
SHIMOSEGAWA Tooru Tohoku Univ., School of Medicine, Assistant Professor, 医学部附属病院, 助手 (90226275)
NAYA K Tohoku Univ., School of Medicine, Assistant Professor
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| Project Period (FY) |
1994 – 1995
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| Keywords | chronic pancreatitis / molecular biology / hereditary disease / familial pancreatitis |
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| Research Abstract |
We studied the genetic abnormality affected the familial chronic pancreatitis (CP) for understanding the pathogenesis of chronic pancreatitis. Wereviewed the reports of familial pancreatitis. Seventy-four hereditary chronic pancreatitis patients from twenty families, in whom pancreatitis occurred in more than two blood-related persons in two and more generations, were reported in Japan. In 70% of them, the onset of pancreatitis is less than twenty years old. Pancreatic calcifications were observed in 46% of cases. Three patients died of pancreatic cancer.
No genetic abnormality in the familial CP has been reported. We determined the HLA antigen and increased frequency of the HLA types DR-2 was seen in fourteen familial CP patients in our clinic.
Genomic DNA was prepared from peripheral lymphocytes and digested with EcoRI,HindIII,BamHI,StagI.Southem blot analysis revealed neither a rearrangement nor a gross deletion of pancreatic secretory trypsin inhibitor (PSTI) and reg I-beta in genomic DNA of affected members of two families. Four exons of PSTI gene amplified by polymerase chain reaction (PCR) from genomic DNA was directly sequenced. One single-base change in the PSTI gene of familial CP patient was observed. But we hava not confirmed this region influenced the synthesis of protein. And we could not find the mutation of whole reg I-beta gene of familial CP patients.
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