臨牀消化器内科 Vol.23 No.3(10)


特集名 胃癌スクリーニングの現況とハイリスクストラテジー
題名 血液検査による胃癌高危険群の集約化
発刊年月 2008年 03月
著者 柳岡 公彦 和歌山県立医科大学第二内科
著者 向林 知津 和歌山県立医科大学第二内科
著者 出口 久暢 和歌山県立医科大学第二内科
著者 前北 隆雄 和歌山県立医科大学第二内科
著者 曲里 浩人 和歌山県立医科大学第二内科
著者 井口 幹崇 和歌山県立医科大学第二内科
著者 玉井 秀幸 和歌山県立医科大学第二内科
著者 有井 研司 和歌山県立医科大学第二内科
著者 岡 政志 和歌山県立医科大学第二内科
著者 一瀬 雅夫 和歌山県立医科大学第二内科
【 要旨 】 血清ペプシノゲン (PG) 検査は,慢性萎縮性胃炎の進展度の判定が可能であり,胃がん検診にも導入され,効率化に貢献している.最近,Helicobacter pylori (H. pylori) 抗体価と併せて用いることで,個人の胃癌リスクを予測することが可能になった.筆者らは,H. pylori感染による胃炎進展,胃癌発生に至る自然史を踏まえ,胃癌高危険群としての萎縮性胃炎の意義をH. pylori感染の各段階について5,209人を対象に,10年間にわたる追跡調査を行い,検討した.H. pylori感染の有無には血清抗H. pylori IgG抗体,慢性萎縮性胃炎の存在および進展度には血清PG値を用いて判定した.これら両検査の結果から,胃癌のほとんどがH. pylori感染に起因する慢性胃炎に由来し,胃炎-萎縮性胃炎・腸上皮化生-胃癌が発生のメインルートであること,H. pylori関連胃炎の進展に伴い胃癌のリスクが段階的に上昇することを明確に示した.
Theme Gastric Cancer Screening -- Present Status and Uprising High-risk Strategy
Title The Two Serum Tests Allow Evaluation of Gastric Cancer Risk in Each Subject and Identification of Individuals at High Risk for the Cancer
Author Kimihiko Yanaoka Second Department of Internal Medicine, Wakayama Medical University
Author Chizu Mukoubayashi Second Department of Internal Medicine, Wakayama Medical University
Author Hisanobu Deguchi Second Department of Internal Medicine, Wakayama Medical University
Author Takao Maekita Second Department of Internal Medicine, Wakayama Medical University
Author Hirohito Magari Second Department of Internal Medicine, Wakayama Medical University
Author Mikitaka Iguchi Second Department of Internal Medicine, Wakayama Medical University
Author Hideyuki Tamai Second Department of Internal Medicine, Wakayama Medical University
Author Kenji Arii Second Department of Internal Medicine, Wakayama Medical University
Author Masashi Oka Second Department of Internal Medicine, Wakayama Medical University
Author Masao Ichinose Second Department of Internal Medicine, Wakayama Medical University
[ Summary ] In high risk areas such as Japan, the main course of stomach carcinogenesis is considered to begin with gastritis, proceeding to extensive atrophy with intestinal metaplasia, then on to dysplasia, and finally to cancer. However, there is controversy as to whether the risk of gastric cancer increases with the progression of atrophy and intestinal metaplasia, which results from gastritis, or whether high levels of gastritis pose a high risk. In order to clarify this point, a longitudinal cohort study over a ten-year period was conducted. The subjects consisted of 5,209 asymptomatic male employees, 40 to 59 years old (average age 49.5 ± 4.6), who underwent an annual multiphasic health checkup in their workplace in Wakayama City, Japan. The subjects were screened annually to identify incident gastric cancer over a 10-year period between 1994 and 2004. Atrophic gastritis was evaluated through endoscopic diagnosis, serum pepsinogen testing and Helicobacter pylori titer measurement. The subjects were divided into four groups labeled A through D [A Group HP (-) PG (-), B Group : HP (+) PG (-), C Group : HP (+) PG (+), D Group : HP (-) PG (+), with the degree of atrophic gastritis being greater sequentially from group A to D, with group D being equivalent to metaplastic gastritis]. In relation to the stage of HP-associated gastritis, 25 cases were in group B, 30 cases in group C, 4 cases in group D. No cancer developed in group A. Thus, the annual incidence of gastric cancer in each group was null in group A, 0.1 % in group B, 0.24 % in group C. and 1.3 % in group D. No gastric cancer developed is HP-free and CAG-free healthy stomachs, while the risk of the cancer increased in a progressive fashion with the progression of HP-associated gastritis.
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