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根除幽门螺杆菌能否预防胃癌?

Can gastric cancer be prevented by Helicobacter pylori eradication?

作者信息

Malfertheiner Peter, Fry Lucia C, Mönkemüller Klaus

机构信息

Division of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Universitätsklinikum Magdeburg, Leipziger Strasse 44, Magdeburg, Germany.

出版信息

Best Pract Res Clin Gastroenterol. 2006;20(4):709-19. doi: 10.1016/j.bpg.2006.04.005.

DOI:10.1016/j.bpg.2006.04.005
PMID:16997155
Abstract

Helicobacter pylori infection always causes chronic gastritis and triggers several gastroduodenal pathologies ranging from peptic ulcer disease to gastric cancer. It is well established that H. pylori eradication decreases the incidence of gastroduodenal ulcer and its recurrence. However, despite being accepted as the critical risk factor for gastric cancer, there is no conclusive evidence that H. pylori eradication decreases the incidence of gastric cancer. Bacterial virulence characteristics, as well as genetic predisposition of the host in conjunction with certain environmental conditions, are the major factors which influence the development of gastric cancer. Preclinical and clinical data suggest that reversibility of precancerous lesions (atrophic gastritis and intestinal metaplasia) is possible in some patients after H. pylori eradication. Since neoplastic lesions do not progress - or even regress in some cases - after H. pylori eradication, eradication therapy should be considered even in patients with precancerous lesions. Nonetheless, progression of atrophic gastritis and intestinal metaplasia into cancer has been also demonstrated in patients after H. pylori eradication, suggesting that there might be a point of no return where genetic changes have already happened and are irreversible despite elimination of the triggering carcinogen (H. pylori). At the present time the clinical decision to treat a patient is based on established risk profiles. A general screen-and-treat policy, although desirable, currently awaits a less complex treatment regimen.

摘要

幽门螺杆菌感染总是会引发慢性胃炎,并引发多种胃十二指肠病变,从消化性溃疡病到胃癌。众所周知,根除幽门螺杆菌可降低胃十二指肠溃疡的发病率及其复发率。然而,尽管幽门螺杆菌被公认为是胃癌的关键危险因素,但尚无确凿证据表明根除幽门螺杆菌可降低胃癌的发病率。细菌毒力特征以及宿主的遗传易感性与某些环境条件共同作用,是影响胃癌发生发展的主要因素。临床前和临床数据表明,在一些患者中,根除幽门螺杆菌后癌前病变(萎缩性胃炎和肠化生)有可能逆转。由于根除幽门螺杆菌后肿瘤性病变不会进展——甚至在某些情况下会消退,因此即使是患有癌前病变的患者也应考虑进行根除治疗。尽管如此,在根除幽门螺杆菌的患者中也已证实萎缩性胃炎和肠化生会发展为癌症,这表明可能存在一个无法回头的临界点,即尽管消除了引发致癌物(幽门螺杆菌),但基因变化已经发生且不可逆转。目前,针对患者的临床治疗决策是基于既定的风险评估。尽管普遍的筛查和治疗策略是可取的,但目前还需要一种更简单的治疗方案。

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Differential inflammatory response to Helicobacter pylori infection: etiology and clinical outcomes.
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J Gastroenterol. 2009;44(1):47-55. doi: 10.1007/s00535-008-2270-x. Epub 2009 Jan 22.
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Evaluation of a commercial immunoblot, Helicoblot 2.1, for diagnosis of Helicobacter pylori infection.评估用于诊断幽门螺杆菌感染的商业免疫印迹法Helicoblot 2.1。
Clin Vaccine Immunol. 2008 Nov;15(11):1705-10. doi: 10.1128/CVI.00165-08. Epub 2008 Sep 30.
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Clin Exp Med. 2008 Mar;8(1):23-9. doi: 10.1007/s10238-008-0152-4. Epub 2008 Apr 3.