臨牀消化器内科 Vol.27 No.3(7)


特集名 H. pylori胃炎からの発癌 ― 除菌有効性を巡っての視点
題名 背景胃粘膜の内視鏡所見と胃癌発生リスク,除菌の効果
発刊年月 2012年 03月
著者 加藤 俊二 日本医科大学外科
著者 松倉 則夫 日本医科大学外科
著者 藤田 逸郎 日本医科大学外科
著者 小野寺 浩之 日本医科大学外科
著者 櫻澤 信行 日本医科大学外科
著者 萩原 信敏 日本医科大学外科
著者 金沢 義一 日本医科大学外科
著者 野村 務 日本医科大学外科
著者 内田 英二 日本医科大学外科
【 要旨 】 H. pylori感染以外の胃発癌リスクとしてBillroth(B) II法術後に多い吻合部周囲の残胃癌は,腸上皮化生を背景粘膜としており,胆汁など十二指腸液の逆流,胃内pHの中性化が原因と考えられ,このことより除菌治療だけでは胃癌発生抑制効果が不十分と考えられる.胃切症例の経年的内視鏡観察による累積再発生率と萎縮性胃炎,腸上皮化生など高危険粘膜を内視鏡生検,ペプシノーゲン法,胃内pHで検討した結果,累積再発生率は有意に粘膜切除を含む局所切除後>B II法後>B I法後の順で高く14.3%,7.5%,1.9%であった.胃癌発生例では組織学的Updated Sydney System 4段階(0〜3)評価でinflammation(炎症によるリンパ球浸潤)がスコア2以上で再発生6例/29例と有意に高く,除菌治療でも慢性炎症が改善しない症例が高リスクと考えられた.炎症,胆汁逆流,胃内中性化の高リスク症例をプロスペクティブに観察して4年後にESD治療を行った症例を提示する.
Theme Carcinogenesis Based on H. pylori-associated Gastritis -- Is Cancer Control Possible by the Eradication ?
Title Causative Factors of Stomach Carcinogenesis after Eradication Therapy for H. pylori Infection
Author Shunji Kato Department of Surgery, Nippon Medical School
Author Norio Matsukura Department of Surgery, Nippon Medical School
Author Itsuo Fujita Department of Surgery, Nippon Medical School
Author Hiroyuki Onodera Department of Surgery, Nippon Medical School
Author Nobuyuki Sakurazawa Department of Surgery, Nippon Medical School
Author Nobutoshi Hagiwara Department of Surgery, Nippon Medical School
Author Yoshikazu Kanazawa Department of Surgery, Nippon Medical School
Author Tsutomu Nomura Department of Surgery, Nippon Medical School
Author Eiji Uchida Department of Surgery, Nippon Medical School
[ Summary ] H. pylori infection is a definite carcinogen leading to stomach carcinogenesis. However, clinically, new or secondary stomach cancers may develop after eradication of H. pylori infection. It is well known that reflux of bile and pancreatic juices, as well as neutralization of pH levels in the stomach, may contribute to production of nitroso-carcinogenic compounds. These compounds may be linked to other carcinogenic factors. We calculated cumulative regenerative morbidity rates in relation to stomach cancer after mucosal resection treatment including endoscopic or local resection. Those rates were higher than those for distal gastrostomy with Billroth II, or Billroth I re-construction procedures, 14.3 %, 7.5 %, 1.9 % respectively. Higher levels of inflammation in the stomach, evaluated from scores derived from the degree of inflammation observed with moderate to severe involvement in the upper segment, without H. pylori infection after the eradication therapy or natural elimination of H. pylori by bile reflux in the mucosa. By comparison, no or only slight inflammation, was found to be more of a risk factor for the development of stomach cancer. It was also seen as a supportive biomarker for the selection of high risk stomach cancer groups. A clinical case for new developments in stomach cancer prediction by this method is exhibited.
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