Biomarkers in Barrett esophagus

Barrett esophagus is a premalignant condition that may progress to adenocarcinoma. The risk of developing cancer has been estimated to be approximately 1 in 250 patient-years of observation; however, there appear to be subsets of patients at much higher risk. Risk stratification has previously been determined by histological identification of dysplasia. Several new biomarkers are being tested to help clinicians better determine the risk of cancer development. Although none of these biomarkers has been proven in a prospective study to predict the onset of cancer, they have been correlated with cancer development. Most of these are factors that have been associated with cancer development in other organs. These include assessment of cell proliferation, expression of cyclooxygenase 2, growth factors and oncogenes, secretory factors, cell cycle proteins, adhesion molecules, and aneuploidy and other genetic abnormalities. In addition to their role as potential cancer biomarkers, these factors have increasingly been reported as surrogate markers to monitor the effectiveness of conservative treatments for Barrett esophagus. In this article, biological markers are reviewed for their relevance in Barrett esophagus. Although most biological markers need to be evaluated further and, for most, prospective follow-up studies are lacking, at present abnormal ploidy status, P16 and P53 gene abnormalities, or allelic losses are the most extensively documented.     

Rationale for surgical therapy of Barrett esophagus

Barrett esophagus has malignant potential and seems to be an acquired abnormality. It is associated with chronic gastroesophageal reflux disease and represents its severest form. The literature comparing medical treatment with antireflux surgery was reviewed. Questions regarding the advantages of surgery, who should undergo surgery, whether surgery can change the course of Barrett esophagus, the change in cancer risk, who needs surveillance, and cost-effectiveness were addressed. The incidence of developing Barrett cancer was 1 in 145 patient-years in reviewing 2032 patient-years of medical therapy compared with 1 in 294 patient-years in reviewing 4122 patient-years after surgery. Median follow-up time in the 2 groups was 2.7 years in the medically treated patients and 4.0 years in the surgically treated patients. Surveillance of Barrett esophagus is required irrespective of treatment. Laparoscopic antireflux surgery was found to be cost-effective after 7 years. Although these data do not prove that surgery is superior to medical treatment in the prevention of cancer related to Barrett esophagus, we found a tendency for surgery to be better than medical therapy to prevent the development and progression of Barrett carcinoma.     

The history of Barrett esophagus

The term Barrett esophagus has become well established in the medical literature to indicate columnar metaplasia of the distal esophagus associated with chronic gastroesophageal reflux disease. However, the historical events that led to the use of this term have become obscured. Here, the historical aspects of Barrett esophagus are reviewed, providing insight not only to this condition but also to the evolution of medical thought in general.     

Pathogenesis of gastroesophageal reflux and Barrett esophagus

Barrett esophagus is a metaplastic condition that affects the lower esophagus and is a complication of gastroesophageal reflux disease (GERD). Under normal circumstances, the reflux of gastric contents into the esophagus is prevented by a complex barrier at the esophagogastric junction. Dysfunction of the lower esophageal sphincter and the presence of a hiatal hernia lead to failure of this barrier. Esophageal mucosal damage results from the chronic exposure of the esophageal mucosa to gastroduodenal contents and the lack of an effective mucosal defense. This article is an overview of the dysfunction of the esophagogastric junction that leads to GERD. The role of the contents of the reflux and that of Helicobacter pylori infection in the pathogenesis of Barrett esophagus are also summarized.     

Revised radiologic concepts of the Barrett esophagus

The radiologic findings in 39 cases of histologically proven Barrett esophagus are reviewed. Esophageal strictures were not found in 18% of the cases, and when present were more often distally located. Esophageal ulcers were found in only 46% of the patients. In 13% of the cases neither ulcer nor stricture was found. The majority (72%) of these cases did not fit the classic stereotype of high esophageal stricture and/or ulcer.Presented at the annual meeting of the American Roentgen Ray Society, Boston, Massachusetts, October 1977     

54例Barrett食管临床研究

目的 分析Barrett食管（barrecc esophagus，BE）患者的临床特点，尤其是胃镜下表现度食管动力改变，以提高BE的诊断率，以期早期治疗。方法 回顾分析54例BE患者的临床资料。结果 22例行食管动力检查提示LESP厦屏障压（LESP-GS）明显降低，酸反流总时间、酸反流总次数以度食管下段pH〈4时间百分比均明显增加。系统治疗后，41例患者在该院行胃镜复诊，21例（51．22％）仍为BE，19例（46．34％）患者恢复正常食管上皮，1例（2．44％）进展为食管腺癌。结论 BE是胃食管反流痛（gastroesophageal reflux disease，GERD）严重的并发症；内镜下治疗联合抑酸治疗为BE治疗提供新的方法。     

Endoscopic and histologic diagnosis of Barrett esophagus

Endoscopy plays an important role in the identification, diagnosis, and treatment of Barrett esophagus. Short-segment (<2-3 cm) and traditional long-segment (>2-3 cm) Barrett esophagus are distinguished solely on the length of metaplastic tissue above the esophagogastric junction. The histologic hallmark of intestinal metaplasia is required to confirm diagnosis. Biopsy specimens obtained from tissue of presumed Barrett esophagus or an irregular Z line confirm metaplastic glandular mucosa and permit evaluation of dysplastic or neoplastic changes. In the appropriate clinical setting, the use of adjunctive diagnostic techniques may facilitate the diagnosis of Barrett esophagus and sequelae such as dysplasia. Chromoendoscopy with high-resolution or magnified endoscopy is simple, safe, and desirable for surveillance but requires additional procedural time. The use of light-induced fluorescence endoscopy and light-scattering spectroscopy (i.e., optical biopsy) is appealing for the diagnosis and characterization of suspicious lesions. Adjunctive endoscopic techniques and adherence to a protocol for performing biopsies facilitate the early detection and subsequent surveillance of Barrett esophagus.     

Photodynamic therapy for dysplastic Barrett esophagus and early esophageal adenocarcinoma

OBJECTIVE: To evaluate our results using photodynamic therapy (PDT) for the treatment of dysplasia or superficial cancer (T1 N0 M0) in patients with Barrett esophagus. PATIENTS AND METHODS: We retrospectively reviewed our clinical experience with 48 patients (34 patients with high-grade dysplasia and 14 patients with superficial cancer in Barrett esophagus) who had been referred for PDT. Initial evaluation included computed tomography and standard and high-frequency catheter endosonography. Follow-up endoscopy was performed 4 to 6 weeks after PDT with ablation of any residual glandular mucosa, using the argon plasma coagulator. Patients were then followed up indefinitely every 3 to 6 months with computed tomography, endosonography, and endoscopic surveillance. RESULTS: The median series follow-up was 18.5 months (range, 1-56 months). Apparent complete photoablation of Barrett mucosa and/or superficial neoplasm was documented in 47 of 48 cases. Complications included symptomatic strictures (11 patients), photosensitivity (7 patients), atrial fibrillation (1 patient) or recurrent congestive heart failure (1 patient), and self-limited esophageal perforation (1 patient). Failure to ablate T1 N0 M0 adenocarcinoma occurred in 1 patient. CONCLUSIONS: Porfimer sodium PDT appears to eradicate dysplastic Barrett mucosa and neoplasia. These results are promising; however, long-term studies are needed to document the efficacy of PDT in reducing the morbidity and mortality in such patients.     

Barrett食管37例临床分析

目的探讨Barrett食管（BE）临床特点及相关致病因素。方法对经胃镜及病理检出的37例Barrett食管进行回顾性分析。结果37例BE病人中有烧心、胸骨后疼痛、反酸等反流性食管炎症状者各占73．0％、64．9％和51．4％，无症状者3例（8．1％）。胃镜下伴有反流性食管炎表现者占89．2％，伴有胆汁反流者7例（18.9％），胃动力减弱者6例（16．2％）。病理检查结果为37例食管下段复层鳞状上皮被柱状上皮取代。结论BE多见于老年人，其发病主要与胃食管反流有关；小部分无明显胃食管反流症状和反流性食管炎胃镜表现的病人，其病因还有待进一步研究。     

套扎辅助内镜下黏膜切除术治疗Barrett食管的前瞻性研究

目的 研究套扎辅助黏膜切除治疗Barrett食管的有效性、安全性。方法 采用前瞻性研究。套扎辅助黏膜切除治疗57例Barrett食管患者。单环或多环套扎器预先吸引病灶形成假息肉,后再通电切除。切除前不予黏膜下注射。术后1个月复查胃镜。结果 57例患者接受套扎辅助黏膜切除,46例为岛型,11例为舌型。舌型组中特殊肠化、异型增生发生率高于岛型组。活检准确率为94.74%。5例术中出血。无狭窄、穿孔发生。结论 套扎辅助黏膜切除用于Barrett食管诊断治疗安全有效。     

Cytologic criteria for the formation of a risk group in Barrett esophagus]

Oncologic screenings of the populations in the areas with increased incidence of esophageal cancer have revealed Barrett's ulcer in 1 percent of the examinees. Endoscopic and cytologic characteristics of this condition are presented. Precancer changes--severe dysplasia--are most frequent in male Kazakhs (14.1 percent) aged 50 to 59 (14.7 percent). Subjects with Barrett's ulcer developing severe dysplasia, as evidenced by cytograms, should be included in the group of subjects at risk for carcinoma of the lower third of the esophagus and cardia.     

双极电凝和抑酸药联用对Barrett食管的治疗价值——附20例次报告

１ 引言 Ｂａｒｒｅｔｔ食管系指食管远端正常的覆层鳞状上皮被特殊的柱状上皮所替代,被认为是一种癌前期的组织学改变。内科治疗目前多数选用抑酸药、Ｈ２受体阻滞药、质子泵抑制药及促胃动力药物,外科则采用贲门成形术。但以上治疗均仅可缓解症状,而无法逆转其肠上皮化生转为Ｂａｒｒｅｔｔ食管的病程［１］。作者根据食管上皮基底细胞在正常酸度环境下可诱导向鳞状上皮转化的原理,在抑酸条件下,采用双极电凝治疗Ｂａｒｒｅｔｔ食管２０例次,取得良好的效果,现报告如下。２资料与方法２．１一般资料 本组１０例为１９９４年１月至…     

An educational tool for photodynamic therapy of Barrett esophagus with high-grade dysplasia: from screening through follow-up.

Photodynamic therapy using a centering balloon was recently approved by the Food and Drug Administration for ablation of Barrett esophagus with high-grade dysplasia. This article is an educational tool for the photodynamic therapy team, addressing four important steps involved with photodynamic therapy: screening for potential patients, patient education, treatment using the centering balloon, and follow-up after treatment. Each step ensures proper care for the patient requiring photodynamic therapy.     

氩离子凝固术治疗巴瑞特食管的临床观察

目的探讨内镜下氩离子凝固术(APC)治疗Barrett食管(BE)的临床疗效。方法选择21003年5月至2004年2月经内镜检查及病理组织学检查诊断的BE患者22例,在内镜下行APC治疗,氩离子凝固治疗单次启动延续时间及启动次数视病灶大小、数目情况而定,一般以内镜下整个病灶凝固为止,所有病例1～3个月内复查内镜。结果22例BE患者中1例失访,1例未到复查时间,其余20例BE患者至复查时17例(85％)胃镜下未见复发,2例在原来部位有散在BE上皮残留,1例在其他部位有新BE上皮生长。结论APC是经内镜非接触性治疗BE的新方法,操作方便,短期疗效较好。     

Short segment Barrett esophagus and specialized columnar mucosa at the gastroesophageal junction

The rising incidence of adenocarcinoma of the esophagus and the gastric cardia has generated interest in the finding of intestinal metaplasia or specialized columnar mucosa in this location. Short segment Barrett esophagus is defined by the presence of columnar-appearing mucosa in the distal esophagus (<3 cm in length) with intestinal metaplasia on biopsy. In contrast, intestinal metaplasia may also be present if biopsy specimens are obtained from a normal-appearing squamocolumnar junction or from the gastric cardia (ie, immediately below the gastroesophageal junction) in the absence of columnar lining of the distal esophagus. This has been termed cardia intestinal metaplasia, gastroesophageal junction intestinal metaplasia, or specialized columnar mucosa at the gastroesophageal junction. This article reviews the currently available data on these rapidly evolving entities of short segment Barrett esophagus and specialized columnar mucosa at the gastroesophageal junction.     

黏膜切除治疗Barrett食管疗效及安全性的Meta分析

目的评价黏膜切除(EMR)对于Barrett食管(BE)治疗的有效性、持久性及不良事件发生率。方法计算机检索Embase、PubMed、维普、中国期刊全文数据库、万方数字化期刊全文数据库等。提取各病理类型的BE接受EMR治疗后根除肠上皮化生(CE-IM)、上皮内瘤变(CE-N)的比率,治疗随访期间肠上皮化(IM)或瘤变复发及不良事件发生率,应用R3.1.3软件合并数据进行统计学分析,计算其有效性、持久性及不良事件发生率。结果共纳入4篇研究,总病例130例。EMR治疗异型增生或黏膜内癌的BE患者中,达到CE-N为97%(95%CI:0.91~0.99),达到CE-IM为91%(95%CI:0.83~0.95),在随访过程中瘤变或IM复发率为8%,常见并发症食管狭窄与出血,其发生率分别为39%和6%。结论 EMR作为BE内镜治疗的推荐方式,其在治疗伴异型增生或黏膜内癌的BE上有确切的效果,但其并发症特别是食管狭窄发生率较高。     

内镜下氩离子凝固术治疗Barrett食管的护理

Barrett食管(Barrett's esophagus,BE )是指食管下段的复层鳞状上皮被化生的单层柱状上皮所替代的一种病理现象,可伴肠化或无肠化.其中伴有肠上皮化生者属于食管腺癌的癌前病变[1].有资料表明,Barrett食管发生恶变的概率比普通人群高30倍～125倍[2,3].