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本文引用的文献

1
Meta-analysis of bismuth quadruple therapy versus clarithromycin triple therapy for empiric primary treatment of Helicobacter pylori infection.铋剂四联疗法与克拉霉素三联疗法经验性治疗幽门螺杆菌感染的荟萃分析。
Digestion. 2013;88(1):33-45. doi: 10.1159/000350719. Epub 2013 Jul 19.
2
Chronic inflammation and oxidative stress: the smoking gun for Helicobacter pylori-induced gastric cancer?慢性炎症和氧化应激:幽门螺杆菌引起胃癌的“罪魁祸首”?
Gut Microbes. 2013 Nov-Dec;4(6):475-81. doi: 10.4161/gmic.25583. Epub 2013 Jun 28.
3
Bismuth-containing quadruple therapy for Helicobacter pylori: lessons from China.含铋四联疗法治疗幽门螺杆菌:来自中国的经验。
Eur J Gastroenterol Hepatol. 2013 Oct;25(10):1134-40. doi: 10.1097/MEG.0b013e3283633b57.
4
Bone marrow-derived mesenchymal stem cells favor the immunosuppressive T cells skewing in a Helicobacter pylori model of gastric cancer.骨髓间充质干细胞有利于在胃癌的幽门螺杆菌模型中偏向免疫抑制性 T 细胞。
Stem Cells Dev. 2013 Nov 1;22(21):2836-48. doi: 10.1089/scd.2013.0166. Epub 2013 Aug 16.
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Clinical application of probiotics in the treatment of Helicobacter pylori infection--a brief review.益生菌在幽门螺杆菌感染治疗中的临床应用——简要综述
J Microbiol Immunol Infect. 2014 Oct;47(5):429-37. doi: 10.1016/j.jmii.2013.03.010. Epub 2013 Jun 10.
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COX-2 regulates E-cadherin expression through the NF-κB/Snail signaling pathway in gastric cancer.COX-2 通过 NF-κB/Snail 信号通路调节胃癌中的 E-钙黏蛋白表达。
Int J Mol Med. 2013 Jul;32(1):93-100. doi: 10.3892/ijmm.2013.1376. Epub 2013 May 10.
7
Gastric cancer chemoprevention: the current evidence.胃癌化学预防:当前证据。
Gastroenterol Clin North Am. 2013 Jun;42(2):299-316. doi: 10.1016/j.gtc.2013.02.001. Epub 2013 Mar 13.
8
Chemoprevention of gastrointestinal cancer: the reality and the dream.胃肠道肿瘤的化学预防:现实与梦想。
Gut Liver. 2013 Mar;7(2):137-49. doi: 10.5009/gnl.2013.7.2.137. Epub 2013 Feb 7.
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Helicobacter pylori infection induced gastric cancer; advance in gastric stem cell research and the remaining challenges.幽门螺杆菌感染导致胃癌;胃干细胞研究的进展及尚存的挑战。
Gut Pathog. 2012 Dec 8;4(1):18. doi: 10.1186/1757-4749-4-18.
10
Sequential versus triple therapy for the first-line treatment of Helicobacter pylori: a multicentre, open-label, randomised trial.序贯与三联疗法一线治疗幽门螺杆菌:一项多中心、开放标签、随机试验。
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非微生物方法治疗幽门螺杆菌比单纯根除更能快速预防胃癌。

Non-microbial approach for Helicobacter pylori as faster track to prevent gastric cancer than simple eradication.

机构信息

Sang-Ho Park, Napapan Kangwan, Jong-Min Park, Eun-Hee Kim, Ki Baik Hahm, CHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul 135-081, South Korea.

出版信息

World J Gastroenterol. 2013 Dec 21;19(47):8986-95. doi: 10.3748/wjg.v19.i47.8986.

DOI:10.3748/wjg.v19.i47.8986
PMID:24379623
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3870551/
Abstract

Although the International Agency for Research on Cancer declared Helicobacter pylori (H. pylori) as a definite human carcinogen in 1994, the Japanese Society for Helicobacter Research only recently (February 2013) adopted the position that H. pylori infection should be considered as an indication for either amelioration of chronic gastritis or for decreasing gastric cancer mortality. Japanese researchers have found that H. pylori eradication halts progressive mucosal damage and that successful eradication in patients with non-atrophic gastritis most likely prevents subsequent development of gastric cancer. However, those who have already developed atrophic gastritis/gastric atrophy retain potential risk factors for gastric cancer. Because chronic perpetuated progression of H. pylori-associated gastric inflammation is associated with increased morbidity culminating in gastric carcinogenesis, a non-microbial approach to treatment that provides long-term control of gastric inflammation through nutrients and other interventions may be an effective way to decrease this morbidity. This non-microbial approach might represent a new form of prerequisite "rescue" therapy that provides a quicker path to the prevention of gastric cancer as compared to simple eradication.

摘要

虽然国际癌症研究机构于 1994 年宣布幽门螺杆菌(H. pylori)为明确的人类致癌物,但日本幽门螺杆菌研究学会直到最近(2013 年 2 月)才采取这一立场,即认为 H. pylori 感染应被视为改善慢性胃炎或降低胃癌死亡率的指征。日本研究人员发现,H. pylori 的根除可阻止进行性黏膜损伤,并且在非萎缩性胃炎患者中成功根除 H. pylori 极有可能预防随后发生胃癌。然而,已经患有萎缩性胃炎/胃萎缩的患者仍然存在胃癌的潜在危险因素。由于与 H. pylori 相关的胃炎症的慢性持续进展与发病率的增加有关,最终导致胃癌变,因此通过营养物质和其他干预措施提供对胃炎症的长期控制的非微生物治疗方法可能是降低这种发病率的有效方法。与单纯根除相比,这种非微生物方法可能代表一种新形式的必要“挽救”疗法,为预防胃癌提供了更快的途径。