Barrett食道癌の組織発生―人体病理と実験病理から

Histogenesis of Barrett's Adenocarcinoma: Analyses of Human Samples and Results of Experimental Animal Studies

要旨　ドイツ人の表在型下部食道腺癌およびその周囲粘膜の解析結果とラット胃・十二指腸液逆流モデルを用いた実験結果に文献的考察を加え，Barrett食道癌の組織発生について考察した．SSBE（short segment Barrett esophagus）にみられるcardiac-type mucosaは，胃側もしくは胃食道接合部に存在する噴門腺が食道側に伸びた胃型粘膜が多い．一方，LSBE（long segment Barrett esophagus）にみられる杯細胞のあるspecialized intestinal metaplasiaは，高濃度の胆汁酸を含む胃液の逆流により発生した化生性の腸型粘膜であり，SSBEより発癌率は高いことが示唆された．

　We discuss the histogenesis of Barrett's adenocarcinoma following the histopathological examination of esophageal adenocarcinoma specimens obtained from the lower esophagus of German individuals. We also include experimental results obtained using rat duodenal contents reflux models. We observed that cardiac-type mucosa in short-segment Barrett's esophagus develops by proliferation of the cardiac glands that exist in the gastric cardia or esophagogastric junction. On the other hand, SIM（specialized intestinal metaplasia）in long-segment Barrett's esophagus occurs through metaplastic change from stem cells located in the basal layer of squamous cell epithelium. This occurs because of esophageal exposure to gastric contents including highly concentrated bile acids. Moreover, the rate of carcinogenesis following SIM in LSBE is higher when compared to that following proliferation of cardiac-type mucosa in SSBE.