1998 Fiscal Year Final Research Report Summary
Analysis of pathophysiology in acute pancreatitis from the stand point of second attack theory
| Project/Area Number |
09470254
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
OGAWA Michio Kumamoto University Medical School, Professor, 医学部, 教授 (30028691)
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| Co-Investigator(Kenkyū-buntansha) |
HIROTA Masahiko Kumamoto University Medical School, 医学部・附属病院, 助手 (80284769)
YAMAGUCHI Yasuo Kumamoto University Medical School, Associate Professor, 医学部, 助教授 (90253757)
MORI Katsutaka Kumamoto University College of Medical Science, Professor, 医療技術短期大学部, 教授 (10040213)
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| Project Period (FY) |
1997 – 1998
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| Keywords | acute pancreatitis / SIRS / cytokine / organ dysfunction / infection / neutrophil / second attack / 重症度評価 |
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| Research Abstract |
Acute pancreatitis is accompanied by destruction and digestion of tissues, causing hvpercytokinemia and hyperreactivity of leukocytes (macrophages and neutrophils) and vascular endothelia! cells. As one of the biological defense mechanisms in this condition, neutrophils infiltrate vital organs, such as lung, liver, and digestive organs. When acute pancreatitis is complicated by infection, hyperreactive macrophages release a large amount of proinflammatory cytokines that activate primed neutrophils as a second attack". Utilizing proteolytic enzymes and oxidant, neutrophils injure the infiltrated vital organs, causing cellular damage and dysfunction of vital organs distant from the pancreas. Multiple organ failure in acute pancreatitis with septic complications can develop, at least in part, by inflammatory cytokine and neutrophil activation.
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