胃癌的高危可控因素——幽门螺杆菌感染

doi:10.3877/cma.j.issn.1674-1358.2023.03.001

幽门螺杆菌感染是消化道溃疡、胃癌以及其他胃疾病的主要致病因素。全球约50%人口受到感染，且存在明显的地区差异。感染主要是经口-口或粪-口途径，病原体可通过改变胃内环境、介导免疫和产生毒力因子，从而成功定植于强酸环境中并发挥致病作用。尽管大多数幽门螺杆菌阳性患者无明显症状，但感染会导致各种胃肠道疾病的发展，致使胃腺癌的发病率进而升高。抗菌药物和铋剂治疗方案在幽门螺杆菌根治中发挥至关重要的作用，但其耐药率高居不下一直为临床治疗中的巨大挑战，这也间接促进了益生菌疗法和相关疫苗研发的进展。由于流行病学条件的变化、具有治疗意义的耐药模式变化以及病原体根治适应证的更新，幽门螺杆菌的医学管理是一个需要定期重新评估的动态过程。本文概述了幽门螺杆菌感染研究现状、致癌机制和治疗方案，重点强调具有高致病性的细菌毒力因子（以cagA和vacA为主）通过可能存在的机制，影响上皮细胞增殖和凋亡间的平衡从而导致癌症发生，旨在提升对幽门螺杆菌感染的认知和防治水平。

关键词: 幽门螺杆菌, 致癌机制, 毒力因子, 根治

Helicobacter pylori (H. pylori) infection is the main pathogenic factor of peptic ulcer, gastric cancer and other gastric diseases. About 50% people worldwide were infected, with significant regional differences. H. pylori infection mainly through oral-oral or fecal-oral route. Pathogens can successfully colonize in strong acid environment and play a pathogenic role in changing the intragastric environment, mediating immunity and producing virulence factors. Although most H. pylori positive patients have no obvious symptoms, the infection will lead to the development of various gastrointestinal diseases, and increases of the incidence of gastric adenocarcinoma. Antibiotics and bismuth agents play a crucial role in the eradication of H. pylori, but the high drug resistance rate has been a great challenge in clinical treatment, which also indirectly promoted the development of probiotics therapy and related vaccines. Due to the change of epidemiological conditions, the change of drug resistance patterns with therapeutic significance and the update of the indications for radical treatment of pathogens, the medical management of H. pylori is a dynamic process that needs to be re-evaluated regularly. This article summarizes the research status, carcinogenic mechanism and treatment of H. pylori infection, and emphasizes the highly pathogenic bacterial virulence factors (mainly including cagA and vacA) affect the balance between epithelial cell proliferation and apoptosis through possible mechanisms which will lead to cancer, inorder to improve the understanding and prevention level of H. pylori infection.

Key words: Helicobacter pylori, Carcinogenic mechanism, Toxicity factor, Eradication treatment

表1 幽门螺杆菌根除指征

根除指征	推荐强度	共识水平（%）
消化性溃疡（无论是否活动和有无并发症）	强	100
胃黏膜相关组织淋巴瘤	强	100
早期胃癌接受内镜下黏膜剥离术或胃次全切除术者	强	100
有胃癌家族史	强	95
计划长期服用非甾体抗炎药（包括低剂量阿司匹林）	强	98
幽门螺杆菌胃炎	强	91
胃增生性息肉	强	93
幽门螺杆菌相关性消化不良	强	91
长期服用质子泵抑制剂	强	88
不明原因的缺铁性贫血	强	100
原发免疫性血小板减少症	强	100
维生素B12缺乏	强	100
证实幽门螺杆菌感染（无根治抗衡因素）	强	100

表1 幽门螺杆菌根除指征

根除指征	推荐强度	共识水平（%）
消化性溃疡（无论是否活动和有无并发症）	强	100
胃黏膜相关组织淋巴瘤	强	100
早期胃癌接受内镜下黏膜剥离术或胃次全切除术者	强	100
有胃癌家族史	强	95
计划长期服用非甾体抗炎药（包括低剂量阿司匹林）	强	98
幽门螺杆菌胃炎	强	91
胃增生性息肉	强	93
幽门螺杆菌相关性消化不良	强	91
长期服用质子泵抑制剂	强	88
不明原因的缺铁性贫血	强	100
原发免疫性血小板减少症	强	100
维生素B12缺乏	强	100
证实幽门螺杆菌感染（无根治抗衡因素）	强	100

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