Barrett食管与食管腺癌

Ｂａｒｒｅｔｔ食管（Ｂａｒｒｅｔｔ＇ｓｅｓｏｐｈａｇｕｓ,ＢＥ）是指食管下段复层鳞状上皮被化生性柱状上皮所取代的病理现象。因ＢＥ是食管腺癌的癌前病变之一,且近年Ｂａｒｒｅｔｔ食管腺癌（下称ＢＥ腺癌）的发病率有增高趋势［１］,因此临床须重视ＢＥ的诊治。ＢＥ的发病机制尚不清楚,在众多的发病因素中,慢性胃食管反流病（ＧＥＲＤ）作为ＢＥ的原发危险因素倍受重视。病理酸反流分三种类型,即直立位反流,卧位反流和联合反流。国内研究提示,卧位反流在ＢＥ的发病过程中起重要作用［２］,然而并非ＧＥＲＤ患者均发展为ＢＥ…     

Barrett食管的新进展

通常认为 Barrett食管大多是继发于胃食管反流病(GERD) ,为一种少见疾病。由于目前临床上 GERD发病率不断增加 ,并且长时间以来未能得到有效治疗 ,使 Barrett食管也呈上升趋势。尽管对 Barrett食管的阐述已有 5 0多年 ,但在临床实际工作中对它的存在及如何确定组织学演化仍然缺乏一致的看法。Barrett食管是指食管粘膜局部的复层鳞状上皮被单层柱状上皮所取代。因为是局灶性而非弥漫性的粘膜改变 ,故称 Barrett上皮化生更为恰当。由于这些单层柱状上皮具有胃或十二指肠粘膜的特点 ,富含杯状细胞 ,具有分泌功能 ,因此同胃十二指肠粘膜一…     

超声内镜诊断Barrett食管的研究进展

Barrett食管(BE)是食管腺癌发病的最危险因素.超声内镜(EUS)能清晰地显示食管壁各层的结构.大量研究表明,EUS可显示BE食管壁黏膜层和黏膜下层增厚,但目前不推荐用EUS诊断BE,和鉴别BE是否存在异型增生.EUS在评估有重度异型增生或有食管黏膜下层癌的BE患者及其食管壁肿瘤侵犯程度和局部淋巴结转移方面有重要意义,虽然其准确性现在还存在争议,但其可为BE患者选择进一步治疗的方案提供重要依据.     

Barrett食管的病理诊断

Barrett食管（BE）作为食管腺癌的癌前病变已得到公认,其正确的病理诊断有助于临床治疗方案的制定和预后评估.本文就BE的病理学特征、病理诊断的影响因素、异型增生诊断的临床意义等问题作一概述,旨在进一步提高临床医师对BE病理诊断的认识.     

Barrett食管及食管腺癌发病机制研究进展

食管腺癌发生率的增长速度居各种癌肿的第二位，目前认为Ｂａｒｒｅｔｔ食管是食管腺癌的一种癌前病变。本就Ｂａｒｒｅｔｔ食管和食管腺癌的关系及食管腺癌的发病机制研究进展作一综述。     

Barrett食管与腺癌的关系

Ｂａｒｒｅｔｔ食管是指食管末端的正常鳞状上皮被有恶性倾向的柱状上皮取代的病理现象 ,其癌变的危险性较一般人群高 30～ 12 5倍[1 5] 。我们通过对不同组织中ｐ2 7ｋｉｐ1及增殖细胞核抗原 (ＰＣＮＡ)表达、ＰＣＮＡ指数的测定 ,旨在揭示食管腺癌、胃食管交界处腺癌的发病机制。一、材料和方法1 实验对象 :收集 1996年 1月 1日～ 2 0 0 0年 6月 1日西安交通大学附属第一、二医院、唐都医院、陕西省肿瘤医院的食管腺癌标本 15例 ,男 8例 ,女 7例 ,平均年龄 (6 1 5± 10 4 )岁 ;胃食管交界处腺癌标本 30例 ,男 2 4例 ,女 6例 ,平均年龄 …     

Barrett食管相关基因研究进展

目前Barrett食管主要靠内镜检查以及活检经病理组织学诊断,由于只有其中较少的一部分会恶变为预后不良的食管腺癌,所以若能准确找出这部分高危人群,提前采取干预措施,将对改善Barrett食管预后具有重要意义.为此,人们试图从微观的基因方面解释这种差异并寻求可靠的生物学标志物以早期检出并提前干预这部分高危人群.此文就近年...     

Barrett食管和食管腺癌的基因表达谱研究

目的:研究Barrett食管(BE)和食管腺癌的基因表达谱,筛查与食管腺癌相关的基因.方法:使用Dchip软件对已经在GEO数据库中公开的BE和食管腺癌Affymetrix芯片表达谱数据进行分析.还原扫描图像进行独立核验,并对基因和组织进行双向聚类,最后用配对t检验筛查出在BE和食管腺癌中表达水平都发生变化的基因,并进一步分析其功能.结果:24张Affymetrix芯片的杂交质量稳定,被污染和发生交叉杂交的探针簇都少于5%.对基因和样本的双向聚类表明,大部分组织分类正确.只有N8和A5位于错误的组织类型中.对其余22张芯片再次分别进行配对t检验,得到24个基因.其中表达水平呈进行性上升的5个,呈进行性下降的19个.新检出的PITX1已在稍前不久的另一项研究中得到证实.结论:用新的分析方法研究已公开的表达谱芯片资料为研究肿瘤的发病机制提供了新的手段.     

Barrett食管的诊断和随访

近 20多年,食管腺癌和贲门癌的发病率在西方国家和亚洲地区均呈上升趋势,尤其是北美和西欧 [1]。食管腺癌的发生和 Barrett食管 (BE)有直接的关系。大量的研究发现,食管末端的腺癌几乎都产生于 BE,而 40％的贲门（胃－食管交界处）癌同 BE有关 [2,3]。 　　一、 BE的定义 :BE是在 1950年由一位名叫 Norman.Barrett的英国心胸外科医生首次报道,并以他的名字命名 [4]。 　　BE的最初定义 [5]：食管远端的正常鳞状上皮被柱状上皮所替代,其受累长度≥ 3cm,也称为长节段 BE（ Long－ segment Barrett's Esophagus,LSBE) [6]。 …     

Barrett食管的研究现状

Barrett食管（BE）是指食管远端复层鳞状上皮被单层柱状上皮所取代的一种病理学现象，又称食管下段柱状上皮化。因为首先是由英国著名的外科医生Dorman Barrett提出，所以后来这种病变即以他的名字命名。BE在欧洲和北美常见，亚洲人和黑人少见。西方国家食管腺癌比鳞癌更常见，在西欧国家近30年来食管腺癌发病率上升了8倍，上升率超过任何一种实体肿瘤。在亚洲食管腺癌也呈上升趋势。BE病人中每年约有0．5％发展为腺癌，由于BE与食管腺癌的发生关系密切，因此，BE成为近年来研究的热点。     

Barrett's食管的研究现状

Barrett's食管是以食管下段逐步肠化及不典型增生为主要特征的食管腺癌癌前状态.本文系统阐述了Barrett's食管定义、发病机制、诊断方法、环氧化酶2(COX-2)等癌基因治疗及内镜下激光、黏膜下切除、光动力治疗等最新进展,为Barrett's食管发病机制的揭示、早期诊断、根治性治疗以及食管腺癌的预防提供了新的思路.     

Biomarkers of Barrett's esophagus

Barrett's esophagus is the strongest risk for esophageal adenocarcinoma(EAC). Metaplasia in patients with BE may progress to dysplasia and then invasive carcinoma. Well-defined diagnostic, progressive, predictive, and prognostic biomarkers are needed to identify the presence of the disease, estimate the risk of malignant transformation, and predict the therapeutic outcome and survival of EAC patients. There are many predictive and prognostic markers that lack substantial validation, and do not allow stratification of patients with gastroesophageal reflux disease in clinical practice for outcome and effectiveness of therapy. In this short review we summarize the current knowledge regarding possible biomarkers, focusing on the pathophysiologic mechanisms to improve prognostic and therapeutic approaches.     

短节段Barrett食管临床研究

目的探讨短节段Barrett食管(SSBE)的临床特征、诊治、随访及其可能发病机制。方法回顾分析52例经内镜和病理确诊的SSBE，重点为内镜特征、病理学改变、食管动力检查结果、内镜复查及疗效观察。结果SSBE内镜下以岛型最多见占86．5％，常规病理证实的特异型肠上皮化生占15．4％，11例患者行24h食管pH和胆汁联合监测及食管测压，72．7％存在异常。21例患者行氩离子凝固术等内镜介入治疗，短期内复查15例SSBE消退。49例复查胃镜者未发现食管癌变。结论SSBE发生与胃酸和胆汁反流相关，内镜下以岛型常见，其肠化生、不典型增生的发生率可能相对较低。     

Dysplasia in Barrett's esophagus

Summary In a retrospective histological study, resected specimens obtained from 23 patients with adenocarcinoma in Barrett's esophagus (Group I) and endoscopic multiple (step) biopsis from 38 patients without carcinoma in Barrett's esophagus (Group II) were investigated for dysplastic changes. Dysplasia was most frequently found in the type of mucosa comprising intestinal metaplasia. There seem to be two pathways to dysplasia in Barrett's esophagus. In Group I dysplasia was found in 18 out of 23, and in Group II in 2 out of 38 patients. In Barrett's esophagus, dysplasia may be considered not only a precursor of carcinoma, but also a marker for coexisting carcinoma.Presented at the 1984 meeting of the American Gastroenterological Association May 20–23, New Orleans, La., USA     

Molecular markers and imaging tools to identify malignant potential in Barrett's esophagus

Due to its rapidly rising incidence and high mortality, esophageal adenocarcinoma is a major public health concern, particularly in Western countries. The steps involved in the progression from its predisposing condition, gastroesophageal reflux disease, to its premalignant disorder, Barrett's esophagus, and to cancer, are incompletely understood. Current screening and surveillance methods are limited by the lack of population-wide utility, incomplete sampling of standard biopsies, and subjectivity of evaluation. Advances in endoscopic ablation have raised the hope of effective therapy for eradication of high-risk Barrett's lesions, but improvements are needed in determining when to apply this treatment and how to follow patients clinically. Researchers have evaluated numerous potential molecular biomarkers with the goal of detecting dysplasia, with varying degrees of success. The combination of biomarker panels with epidemiologic risk factors to yield clinical risk scoring systems is promising. New approaches to sample tissue may also be combined with these biomarkers for less invasive screening and sur-veillance. The development of novel endoscopic imaging tools in recent years has the potential to markedly improve detection of small foci of dysplasia in vivo. Current and future efforts will aim to determine the combination of markers and imaging modalities that will most effectively improve the rate of early detection of highrisk lesions in Barrett's esophagus.     

Lugol液染色诊断Barrett食管的临床价值

目的 通过Lugol液染色后取活检提高Barrett食管（BE）的诊断率。方法 内镜下考虑Barrett食管患者72例，其中37例接受Lugol液染色后取活检，35例常规内镜下取活检。结果 Lugol液染色后取活检诊断BE的敏感性、特异性、阳性预测值（PPV）、阴性预测值（NPV）分别为72．22％、78．94％、76．47％、75．00％。常规内镜下取活检诊断BE的敏感性、特异性、阳性预测值、阴性预测值分别为37．50％、63．15％、46．15％、54．54％。结论 Lugol液染色后取活检有助于提高Barrett食管的诊断率。     

内镜下氩离子凝固术治疗Barrett食管

目的对氩离子凝固术（APC）治疗Barrett食管（BE）的疗效进行前瞻性评估。方法选择2004年3月至2005年1月经胃镜检查、病理证实的15例BE患者进行60WAPC治疗，术后予质子泵抑制剂辅助治疗。对其疗程、疗效、并发症进行评估。结果15例均完成治疗，平均随访期为13．2个月。12例仅需1次APC治疗即获得消除，3例需2次治疗，平均烧灼次数为1．2次。8例治疗期间有轻度并发症，其中7例为胸骨后疼痛，1例治疗后出现轻度吞咽困难，未予手术治疗，半年后逐步缓解。1例在BE完全消除后6个月再现肠上皮化生，该例患者再次予以APC治疗，之后6个月内2次胃镜检查未发现复发，治疗总有效率为93％。结论APC治疗是一种安全、有效的治疗BE的方法。     

长、短节段Barrett食管胃镜表现与病理特征对比分析

目的 探讨长、短节段Barrett食管胃镜表现和病理特征的异同.方法 回顾分析128例经胃镜和病理学诊断确诊的Barrett食管,其中长节段Barrett食管（LSBE）40例,短节段Barrett食管（SSBE）88例,重点分析两者在年龄分布、性别构成、胃镜表现及病理诊断的异同点.数据行t检验及u检验.结果LSBE组与SSBE组在年龄分布、性别构成上无差异（P＞0.05）.胃镜下LSBE组以全周型最多见,占62.5%;SSBE组以岛型最多见,占85.2%.LSBE组特异型肠上皮化生的发生率比SSBE组明显增高,差异有统计学意义（47.5%比14.8%,P＜0.01）.在特异型肠上皮化生中,LSBE组轻、中、重度不典型增生的发生率（15.0%,12.5%,5.0%）较SSBE组（4.5%,3.4%,0.0%）高,差异也具有统计学意义（P值均＜0.05）.结论 LSBE较SSBE更易发生不典型增生,应充分认识胃镜表现结合病理诊断的重要性。     

Long-term follow-up after complete ablation of Barrett＇s esophagus with argon plasma coagulation

AIM: To report the long-term outcome of patients after complete ablation of non-neoplastic Barrett's esophagus (BE) with respect to BE relapse and development of intraepithelial neoplasia or esophageal adenocarcinoma. METHODS: In 70 patients with historically proven non neoplastic BE, complete BE ablation was achieved by argon plasma coagulation (APC) and high-dose proton pump inhibitor therapy (120 mg omeprazole daily). Sixty-six patients (94.4%) underwent further surveillance endoscopy. At each surveillance endoscopy four-quadrant biopsies were taken from the neo-squamous epithelium at 2 cm intervals depending on the pre-treatment length of BE mucosa beginning at the neo-Z-line, and from any endoscopically suspicious lesion. RESULTS: The median follow-up of 66 patients was 51 mo (range 9-85 mo) giving a total of 280.5 patient years. A mean of 6 biopsies were taken during surveillance endoscopies. In 13 patients (19.7%) tongues or islands suspicious for BE were found during endoscopy. In 8 of these patients (12.1%) non-neoplastic BE relapse was confirmed histologically giving a histological relapse rate of 3% per year. In none of the patients, intraepithelial neoplasia nor an esophageal adenocarcinoma was detected. Logistic regression analysis identified endoscopic detection of islands or tongues as the only positive predictor of BE relapse (P= 0.0004). CONCLUSION: The long-term relapse rate of non neoplastic BE following complete ablation with high-power APC is low (3% per year).     

Optical molecular imaging for detection of Barrett's-associated neoplasia

Recent advancements in the endoscopic imaging of Barrett's esophagus can be used to probe a wide range of optical properties that are altered with neoplastic progression.This review summarizes relevant changes in optical properties as well as imaging approaches that measures those changes.Wide-field imaging approaches include narrow-band imaging that measures changes in light scattering and absorption,and autofluorescence imaging that measure changes in endogenous fluorophores.High-resolution imaging approa...