セッション情報 International Forum 1(Gastrointestinal tract) 3.Pathogenesis of NSAIDs-enteropathy

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IF1-3-II (Keynote lecture) Prostaglandins and Non-steroidal Anti-inflammatory Drug induced Enteropathy

演者 Masahiro Igarashi(Cancer Institute Hospital of JFCR^1)
共同演者 Kiyonori Kobayashi(Kitasato University East Hospital TokyoJapan^2)
抄録 Non-steroidal anti-inflammatory drug (NSAID) is known to increase the risk of small intestine and colon.The NSAID induced intestinal lesions was diagnosed by the exclusion of the other disease and strong rela-tion to NSAID administration. Thirteen men and 10 women were diagnosed based on our criteria Thecharacteristics of short term NSAID induced lesions which was defined as administration of drugs lessthan one month were as follows : The chief complaint was hematocheziathe lesions were often multiplethe ulcers were round and punched out with friableand the lesions were frequently located on the ileoce-cal valve and terminal ileum. Shortest duration of NSAID administration was three days before the dis-ease appeared. ln cases of long-term administration (more than one month)complains were diarrheawith abdominal pain and hemorrhage. The lesions of long-term administration were round ulcers withstricture. The pathogenesis of NSAID induced enteropathy is not clear. Howeverfrom conventionalstudythe following hypotheses are shown. Firstcyclooxygenase-independent mechanism which was aninj ury assumes mitochondria and increasing permeability and bring about mucosal damages. Second is cy-clooxygenaze-mediated mechanism which causes an obstacle of a cell by NSAID inhibits COX activityand suppressed prostaglandin synthesis in a mucous membraneand it is assumed that a mucosal injuryoccurs by increasing permeabilitya bacterial invasion. ln an above clinical caseswe have experienced thecases that accepted improvement of lesions by administering a prostaglandin drug (Misoprostol) contrib-utes to protect intestinal mucosal damages.We consider it mainly on NSAID induced enteropathy and relation with prostaglandin.
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