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十二指肠胃反流与残胃癌

Duodenogastric reflux and gastric stump carcinoma.

作者信息

Kondo Ken

机构信息

Deptartment of Surgery, Nagoya National Hospital, 1-1 San-nomaru 4-chome, Naka-ku, Nagoya 460-0001, Japan.

出版信息

Gastric Cancer. 2002;5(1):16-22. doi: 10.1007/s101200200002.

DOI:10.1007/s101200200002
PMID:12021855
Abstract

Gastric stump carcinoma after gastric surgery for benign disease is now widely recognized as a distinct clinical entity. The stump carcinoma was often found to be localized to the anastomosis, known to be the site with severe duodenogastric reflux. For this reason, duodenogastric reflux, including the reflux of bile and pancreatic juice, after a Billroth II procedure for benign disease is frequently discussed as an important factor related to the development of stump carcinoma. Many experiments have implicated bile acids, the main component of the duodenal juice, in gastric carcinogenesis. In particular, rat models without the use of the carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), showed adenocarcinoma in the remnant stomach that was related to the severity of duodenogastric reflux. However, human data are, inevitably, much less consistent. Whether the incidence of stump carcinoma is higher than that of gastric carcinoma in general is still controversial. Concerning the histogenesis of stump carcinoma after benign disease, a relationship between gastritis cystica polyposa (GCP) and gastric type adenocarcinoma has been suggested. Recently, the population at risk of gastric stump carcinoma for benign disease has been diminishing significantly, and the incidence of gastric stump carcinoma after surgery for malignant disease has been increasing. The influence of duodenogastric reflux in the gastric remnant after malignant disease may differ from its influence in the gastric remnant after benign disease. Further clinical study is needed to elucidate the pathogenetic factors involved in gastric stump carcinoma.

摘要

良性疾病胃手术后发生的残胃癌目前已被广泛认为是一种独特的临床实体。残胃癌常被发现局限于吻合口,而吻合口是十二指肠胃反流严重的部位。因此,良性疾病毕Ⅱ式手术后的十二指肠胃反流,包括胆汁和胰液反流,常被作为与残胃癌发生相关的重要因素进行讨论。许多实验表明十二指肠液的主要成分胆汁酸与胃癌发生有关。特别是在未使用致癌物N-甲基-N'-硝基-N-亚硝基胍(MNNG)的大鼠模型中,残胃出现了与十二指肠胃反流严重程度相关的腺癌。然而,人体数据不可避免地缺乏一致性。残胃癌的发病率是否总体上高于胃癌仍存在争议。关于良性疾病后残胃癌的组织发生,有人提出胃息肉样囊肿性胃炎(GCP)与胃型腺癌之间存在关联。近年来,良性疾病残胃癌的高危人群已显著减少,而恶性疾病手术后残胃癌的发病率却在上升。恶性疾病后胃残端十二指肠胃反流的影响可能与良性疾病后胃残端的影响不同。需要进一步的临床研究来阐明残胃癌的致病因素。

相似文献

1
Duodenogastric reflux and gastric stump carcinoma.十二指肠胃反流与残胃癌
Gastric Cancer. 2002;5(1):16-22. doi: 10.1007/s101200200002.
2
Possible role of duodenogastric reflux on the development of remnant gastric carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats.十二指肠-胃反流在N-甲基-N'-硝基-N-亚硝基胍诱导的大鼠残胃癌发生中的可能作用。
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Duodenogastric reflux and foregut carcinogenesis.十二指肠-胃反流与前肠致癌作用
Cancer. 1995 Mar 15;75(6 Suppl):1426-32. doi: 10.1002/1097-0142(19950315)75:6+<1426::aid-cncr2820751506>3.0.co;2-#.
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Duodenogastric reflux and gastric mucosal polyamines in the non-operated stomach and in the gastric remnant after Billroth II gastric resection. A role in gastric carcinogenesis?毕Ⅱ式胃切除术后非手术胃及胃残端中的十二指肠-胃反流与胃黏膜多胺。在胃癌发生中起作用?
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Gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine: role of gastrectomy and duodenal reflux.N-甲基-N'-硝基-N-亚硝基胍诱导的胃癌发生:胃切除术和十二指肠反流的作用
Jpn J Cancer Res. 1985 Mar;76(3):167-72.
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[Carcinogenicity of duodenogastric reflux juice in patients undergoing gastrectomy].[胃切除术后患者十二指肠胃反流液的致癌性]
Zhonghua Wai Ke Za Zhi. 2001 Oct;39(10):764-6.
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Pathogenesis of adenocarcinoma induced by gastrojejunostomy in Wistar rats: role of duodenogastric reflux.Wistar大鼠胃空肠吻合术后腺癌的发病机制:十二指肠-胃反流的作用
Carcinogenesis. 1995 Aug;16(8):1747-51. doi: 10.1093/carcin/16.8.1747.
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[The influence of reflux of bile and pancreatic juice on gastric carcinogenesis in rats].[胆汁和胰液反流对大鼠胃癌发生的影响]
Nihon Geka Gakkai Zasshi. 1990 Jul;91(7):818-26.
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Correlation between duodenogastric reflux and remnant gastritis after distal gastrectomy.远端胃切除术后十二指肠-胃反流与残胃炎的相关性
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Promotion of gastric tumorigenesis by duodenal contents in rats induced with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).用N-甲基-N'-硝基-N-亚硝基胍(MNNG)诱导的大鼠中十二指肠内容物促进胃肿瘤发生
Surgery. 1988 Jun;103(6):643-7.

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