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幽门螺杆菌根除后胃癌发生风险

Risk of gastric cancer development after eradication of Helicobacter pylori.

作者信息

Cheung Ka-Shing, Leung Wai K

机构信息

Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.

出版信息

World J Gastrointest Oncol. 2018 May 15;10(5):115-123. doi: 10.4251/wjgo.v10.i5.115.

DOI:10.4251/wjgo.v10.i5.115
PMID:29770171
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5952268/
Abstract

() infection is the most important risk factor for gastric cancer (GC) development through the Correa's gastric carcinogenesis cascade. However, eradication alone does not eliminate GC, as pre-neoplastic lesions (atrophic gastritis, intestinal metaplasia and dysplasia) may have already developed in some patients. It is therefore necessary to identify patients at high-risk for gastric cancer after eradication to streamline the management plan. If the patients have not undergone endoscopy with histologic assessment, the identification of certain clinical risk factors and non-invasive testing (serum pepsinogen) can predict the risk of atrophic gastritis. For those with suspected atrophic gastritis, further risk stratification by endoscopy with histologic assessment according to validated histologic staging systems would be advisable. Patients with higher stages may require long-term endoscopic surveillance. Apart from secondary prevention to reduce deaths by diagnosing GC at an early stage, identifying medications that could potentially modify the GC risk would be desirable. The potential roles of a number of medications have been suggested by various studies, including proton pump inhibitors (PPIs), aspirin, statins and metformin. However, there are currently no randomized clinical trials to address the impact of these medications on GC risk after eradication. In addition, most of these studies failed to adjust for the effect of concurrent medications on GC risk. Recently, large population-based retrospective cohort studies have shown that PPIs were associated with an increased GC risk after eradication, while aspirin was associated with a lower risk. The roles of other agents in reducing GC risk after eradication remain to be determined.

摘要

()感染是通过科雷亚胃癌发生级联导致胃癌(GC)发生的最重要风险因素。然而,单纯根除并不能消除胃癌,因为在一些患者中可能已经出现了癌前病变(萎缩性胃炎、肠化生和发育异常)。因此,有必要识别根除幽门螺杆菌后胃癌高危患者,以优化管理方案。如果患者尚未接受组织学评估的内镜检查,确定某些临床风险因素和非侵入性检测(血清胃蛋白酶原)可以预测萎缩性胃炎的风险。对于疑似萎缩性胃炎的患者,根据经过验证的组织学分期系统进行组织学评估的内镜检查进一步风险分层是可取的。较高分期的患者可能需要长期内镜监测。除了通过早期诊断胃癌来降低死亡率的二级预防外,确定可能改变胃癌风险的药物也是可取的。各种研究提出了多种药物的潜在作用,包括质子泵抑制剂(PPI)、阿司匹林、他汀类药物和二甲双胍。然而,目前尚无随机临床试验来探讨这些药物对根除幽门螺杆菌后胃癌风险的影响。此外,这些研究大多未能调整同时使用的药物对胃癌风险的影响。最近,基于人群的大型回顾性队列研究表明,根除幽门螺杆菌后PPI与胃癌风险增加相关,而阿司匹林与较低风险相关。其他药物在根除幽门螺杆菌后降低胃癌风险中的作用仍有待确定。

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