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Natural history of Barrett's esophagus.巴雷特食管的自然史。
World J Gastroenterol. 2012 Jul 21;18(27):3483-91. doi: 10.3748/wjg.v18.i27.3483.
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Distribution of body fat and its influence on esophageal inflammation and dysplasia in patients with Barrett's esophagus.体脂肪分布及其对巴雷特食管患者食管炎症和异型增生的影响。
Clin Gastroenterol Hepatol. 2012 Jul;10(7):728-34; quiz e61-2. doi: 10.1016/j.cgh.2012.03.007. Epub 2012 Mar 17.
3
Validation of the Prague C & M criteria for the endoscopic grading of Barrett's esophagus by gastroenterology trainees: a multicenter study.《由胃肠病学实习医生验证布拉格 C&M 标准对 Barrett 食管的内镜分级的准确性:一项多中心研究》
Gastrointest Endosc. 2012 Feb;75(2):236-41. doi: 10.1016/j.gie.2011.09.017.
4
Risk factors for neoplastic progression in Barrett's esophagus.巴雷特食管癌变的危险因素。
World J Gastroenterol. 2011 Aug 28;17(32):3672-83. doi: 10.3748/wjg.v17.i32.3672.
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Helicobacter pylori infection and the risks of Barrett's oesophagus: a population-based case-control study.幽门螺杆菌感染与 Barrett 食管风险:基于人群的病例对照研究。
Int J Cancer. 2012 May 15;130(10):2407-16. doi: 10.1002/ijc.26242. Epub 2011 Aug 17.
6
The minimal incubation period from the onset of Barrett's oesophagus to symptomatic adenocarcinoma.从 Barrett 食管发病到有症状的腺癌的最短潜伏期。
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7
Gastroesophageal reflux disease in Asia: A historical perspective and present challenges.亚洲胃食管反流病:历史透视与当前挑战。
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Low-grade dysplasia in Barrett's esophagus: overdiagnosed and underestimated.巴雷特食管低级别上皮内瘤变:过度诊断和低估。
Am J Gastroenterol. 2010 Jul;105(7):1523-30. doi: 10.1038/ajg.2010.171. Epub 2010 May 11.
9
Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia.不同国家食管和胃疾病定义的差异:食管胃交界的内镜定义、Barrett 腺癌前体、Barrett 食管的定义,以及黏膜腺癌或高级别上皮内瘤变的组织学标准。
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10
Esophageal adenocarcinoma in Barrett's esophagus after endoscopic ablative therapy: a meta-analysis and systematic review.内镜消融治疗后巴雷特食管中的食管腺癌:一项荟萃分析和系统评价
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与巴雷特上皮发育异常相关的危险因素。

Risk factors associated with Barrett's epithelial dysplasia.

作者信息

Fujita Mikiko, Nakamura Yuri, Kasashima Saeko, Furukawa Maiko, Misaka Ryoichi, Nagahara Hikaru

机构信息

Mikiko Fujita, Yuri Nakamura, Saeko Kasashima, Maiko Furukawa, Ryoichi Misaka, Hikaru Nagahara, Department of Gastroenterology, Aoyama Hospital, Tokyo Women's Medical University, Tokyo 1070061, Japan.

出版信息

World J Gastroenterol. 2014 Apr 21;20(15):4353-61. doi: 10.3748/wjg.v20.i15.4353.

DOI:10.3748/wjg.v20.i15.4353
PMID:24764673
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3989971/
Abstract

AIM

To elucidate risk factors associated with dysplasia of short-segment Barrett's esophagus (BE).

METHODS

A total of 151 BE patients who underwent endoscopic examination from 2004 to 2008 in Aoyama Hospital, Tokyo Women's Medical University, Japan and whose diagnosis was confirmed from biopsy specimens were enrolled in the study. BE was diagnosed based on endoscopic findings of gastric-appearing mucosa or apparent columnar-lined esophagus proximal to the esophagogastric junction. Dysplasia was classified into three grades - mild, moderate and severe - according to the guidelines of the Vienna Classification System for gastrointestinal epithelial neoplasia. Anthropometric and biochemical data were analyzed to identify risk factors for BE dysplasia. The prevalence of Helicobacter pylori (H. pylori) infection and the expression of p53 by immunohistological staining were also investigated.

RESULTS

Histological examination classified patients into three types: specialized columnar epithelium (SCE) (n = 65); junctional (n = 38); and gastric fundic (n = 48). The incidence of dysplasia or adenocarcinoma from BE of the SCE type was significantly higher than that of the other two types (P < 0.01). The univariate analysis revealed that sex, H. pylori infection, body weight, p53 overexpression, and low diastolic blood pressure (BP) were associated with BE dysplasia. In contrast, body mass index, waist circumference, metabolic syndrome complications, and variables related to glucose or lipid metabolism were not associated with dysplasia. Multivariate logistic analysis showed that overexpression of p53 [odds ratio (OR) = 13.1, P = 0.004], H. pylori infection (OR = 0.19, P = 0.066), and diastolic BP (OR = 0.87, P = 0.021) were independent risk factors for epithelial dysplasia in BE patients with the SCE type.

CONCLUSION

Overexpression of p53 is a risk factor for dysplasia of BE, however, H. pylori infection and diastolic BP inversely associated with BE dysplasia might be protective.

摘要

目的

阐明与短节段巴雷特食管(BE)发育异常相关的危险因素。

方法

本研究纳入了2004年至2008年在日本东京女子医科大学青山医院接受内镜检查且活检标本确诊的151例BE患者。BE根据胃黏膜样黏膜或食管胃交界处近端明显的柱状上皮食管的内镜检查结果进行诊断。根据胃肠道上皮肿瘤维也纳分类系统的指南,发育异常分为轻度、中度和重度三级。分析人体测量和生化数据以确定BE发育异常的危险因素。还研究了幽门螺杆菌(H. pylori)感染的患病率以及通过免疫组织化学染色检测的p53表达。

结果

组织学检查将患者分为三种类型:特殊柱状上皮(SCE)(n = 65);交界型(n = 38);和胃底型(n = 48)。SCE型BE发生发育异常或腺癌的发生率显著高于其他两种类型(P < 0.01)。单因素分析显示,性别、H. pylori感染、体重、p53过表达和低舒张压(BP)与BE发育异常有关。相比之下,体重指数、腰围、代谢综合征并发症以及与葡萄糖或脂质代谢相关的变量与发育异常无关。多因素逻辑分析表明,p53过表达[比值比(OR)= 13.1,P = 0.004]、H. pylori感染(OR = 0.19,P = 0.066)和舒张压(OR = 0.87,P = 0.021)是SCE型BE患者上皮发育异常的独立危险因素。

结论

p53过表达是BE发育异常的危险因素,然而,与BE发育异常呈负相关的H. pylori感染和舒张压可能具有保护作用。