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.     

多环黏膜切除术治疗Barrett食管的临床研究

目的研究内镜下应用多环黏膜切除术（multiband mucosectomy,MBM）治疗Barrett食管。方法采用前瞻性研究的方法,在窄波成像（narrow band imaging,NBI）下确认Barrett食管病变范围,用多环黏膜切除器吸引病灶,套扎橡皮圈后用圈套器电切。3个月复查胃镜,评估疗效。结果134例Barrett食管患者共切除病灶206块。急性并发症出血发生率6.7%（9/134）,无一例发生穿孔。术后30d内（迟发性并发症）出血发生率1.5%（2/134）,出现食管狭窄症状39.8%（53/133）;30d后（远期并发症）主要为食管狭窄,发生率2.3%（3/133）。术后3个月复查胃镜,病灶完整切除率98.5%（131/133）。结论内镜下MBM术治疗Barrett食管,简便、安全、有效。     

Barrett Esophagus

Barrett esophagus is a metaplastic change in the lining of the distal esophageal epithelium, characterized by replacement of the normal squamous epithelium by specialized intestinal metaplasia. The presence of Barrett esophagus increases the risk of esophageal adenocarcinoma several-fold. Esophageal adenocarcinoma is a malignancy with rapidly rising incidence and persistently poor outcomes when diagnosed after the onset of symptoms. Risk factors for Barrett esophagus include chronic gastroesophageal reflux, central obesity, white race, male gender, older age, smoking, and a family history of Barrett esophagus or esophageal adenocarcinoma. Screening for Barrett esophagus in those with several risk factors followed by endoscopic surveillance to detect dysplasia or adenocarcinoma is currently recommended by society guidelines. Minimally invasive nonendoscopic tools for the early detection of Barrett esophagus are currently being developed. Multimodality endoscopic therapy—using a combination of endoscopic resection and ablation techniques—for the treatment of dysplasia and early adenocarcinoma is successful in eliminating intestinal metaplasia and preventing progression to adenocarcinoma, with outcomes comparable to those after esophagectomy. Risk stratification of those diagnosed with Barrett esophagus is a challenge at present, with active research focused on identifying clinical and biomarker panels to identify those with low and high risk of progression. This narrative review highlights some of the challenges and recent progress in this field.     

Controversies in Barrett Esophagus

Barrett esophagus develops when metaplastic columnar epithelium predisposed to develop adenocarcinoma replaces esophageal squamous epithelium damaged by gastroesophageal reflux disease. Although several types of columnar metaplasia have been described in Barrett esophagus, intestinal metaplasia with goblet cells currently is required for a definitive diagnosis in the United States. Studies indicate that the risk of adenocarcinoma for patients with nondysplastic Barrett esophagus is only 0.12% to 0.38% per year, which is substantially lower than previous studies had suggested. Nevertheless, the incidence of esophageal adenocarcinoma continues to rise at an alarming rate. Regular endoscopic surveillance for dysplasia is the currently recommended cancer prevention strategy for Barrett esophagus, but a high-quality study has found no benefit of surveillance in preventing deaths from esophageal cancer. Medical societies currently recommend endoscopic screening for Barrett esophagus in patients with multiple risk factors for esophageal adenocarcinoma, including chronic gastroesophageal reflux disease, age of 50 years or older, male sex, white race, hiatal hernia, and intra-abdominal body fat distribution. However, because the goal of screening is to identify patients with Barrett esophagus who will benefit from endoscopic surveillance and because such surveillance may not be beneficial, the rationale for screening might be made on the basis of faulty assumptions. Endoscopic ablation of dysplastic Barrett metaplasia has been reported to prevent its progression to cancer, but the efficacy of endoscopic eradication of nondysplastic Barrett metaplasia as a cancer preventive procedure is highly questionable. This review discusses some of these controversies that affect the physicians and surgeons who treat patients with Barrett esophagus. Studies relevant to controversial issues in Barrett esophagus were identified using PubMed and relevant search terms, including Barrett esophagus, ablation, dysplasia, radiofrequency ablation, and endoscopic mucosal resection.     

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。     

Barrett's esophagus occurring as a complication of scleroderma

Two patients had both scleroderma and a columnar epithelium-lined lower esophagus (Barrett esophagus). Features of Barrett's esophagus included high esophageal strictures in both patients and ulcer craters in the columnar area of one. Biopsy confirmed columnar epithelium in the lower esophagus of each patient. In these patients, the Barrett esophagus probably was a complication of scleroderma and resulted from long-standing gastroesophageal reflux.     

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.     

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.     

Barrett食管治疗的临床证据

目的针对Barrett食管的治疗方法，进行证据检索和评价，为临床医生和患者提供有关Barrett食管治疗的最新循证医学证据。 方法计算机检索MEDLINE（1978～2006）、CBMdisc（1978～2006）及Cochrane图书馆（2005年第3期），查找与Barrett食管治疗有关的临床随机对照试验、系统评价等，并对所搜集的证据进行评价。 结果Barrett食管的治疗方法包括饮食干预、改变生活方式、药物治疗、内镜下治疗及外科手术治疗等，可依据患者病情选择不同治疗方法。 结论内镜下治疗已取得很大进展，多种治疗方法联用可取得良好效果。     

无痛胃镜下氩气刀治疗Barrett食管的护理

Barrett食管（Barrett’s Esophagus,BE）是慢性胃食管返流致食管下段的复层鳞状上皮损伤后被柱状上皮所代替的一种病理改变。BE是食管癌的癌前病变,其发病率为正常人群30-50倍。因此阻断BE的进展,     

Poor results of 5-aminolevulinic acid-photodynamic therapy for residual high-grade dysplasia and early cancer in barrett esophagus after endoscopic resection

BACKGROUND AND STUDY AIMS: The aim of the study was to evaluate the efficacy of photodynamic therapy (PDT) in the treatment of residual high-grade dysplasia or early cancer (HGD/EC) after endoscopic resection in Barrett esophagus. PATIENTS AND METHODS: Study patients were separated into group A, with proven residual HGD/EC, and group B with possible HGD/EC (positive lateral margins in the endoscopic resection specimen, without HGD/EC in the remaining Barrett esophagus). PDT treatment consisted of 5-aminolevulinic (5-ALA) photosensitization (40 mg/kg) followed by illumination of the Barrett esophagus with a total light dose of 100 J/cm (2). Complete remission was defined as the absence of HGD/EC in biopsies taken in two consecutive follow-up endoscopies. The percentage regression of Barrett esophagus, as well as the recurrence rate of HGD/EC, was calculated. RESULTS: 20 patients underwent PDT (group A, 11; group B, 9). Mild complications were seen in 4/26 procedures. The overall success rate was 15/20 (75 %). There was a significant difference in success rate between group A (55 %) and group B (100 %); P = 0.03. All patients had residual Barrett esophagus after PDT; the median regression percentage was 50 % (IQR 25 - 70 %). Recurrence of HGD/EC occurred in four patients (two each in groups A and B) after a median follow up of 30 months. CONCLUSIONS: In this selected group of patients, the addition of 5-ALA-PDT after endoscopic resection for HGD/EC had a disappointing success rate in patients who had residual HGD/EC after endoscopic resection. Most patients undergoing 5-ALA-PDT have residual Barrett mucosa after PDT and 5-ALA-PDT does not seem to prevent recurrences during follow-up.     

Barrett esophagus: update for radiologists

Barrett esophagus is a well-recognized entity in which there is progressive columnar metaplasia of the lower esophagus due to longstanding gastroesophageal reflux and reflux esophagitis [1]. This condition is important because it is associated with an increased risk of developing esophageal adenocarcinoma by a well-established sequence from dysplasia to carcinoma [2]. During the past decade, however, an explosion of new data has dramatically affected our understanding of Barrett esophagus. Not only have revised histopathologic criteria been developed for this condition, but it is currently believed that patients with Barrett esophagus should be classified as having short-segment or long-segment disease based on the extent of columnar metaplasia in the distal esophagus. This distinction has important implications for the risk of developing esophageal adenocarcinoma and subsequent need for endoscopic surveillance. The purpose of this article is to present these new concepts about Barrett esophagus and provide radiologists with a more current framework for diagnosing this condition.     

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。     

Esophageal dysmotility in patients undergoing photodynamic therapy

OBJECTIVE: To study the esophageal motility of patients with esophageal adenocarcinoma or Barrett esophagus with high-grade dysplasia before and after photodynamic therapy. PATIENTS AND METHODS: In this prospective study conducted between January 1998 and October 1999, esophageal motility testing of the lower esophageal sphincter and esophageal body was performed with a water-perfused catheter, 2 days before and at least 3 weeks after patients underwent photodynamic therapy for esophageal adenocarcinoma or Barrett esophagus. Results were classified as normal motility, ineffective esophageal motility, or aperistalsis. RESULTS: Twenty-three patients were studied, 13 with carcinoma and 10 with Barrett esophagus. Overall, 11 patients (48%) had normal motility, 6 (26%) had ineffective esophageal motility, and 6 (26%) had aperistalsis. Five patients with aperistalsis had carcinoma. Follow-up tracings after photodynamic therapy found that 6 patients (26%) had normal motility, 7 (30%) had ineffective esophageal motility, and 10 (43%) had aperistalsis. CONCLUSIONS: Esophageal dysmotility is common in patients with esophageal adenocarcinoma or Barrett esophagus. Photodynamic therapy may worsen esophageal motility in some patients. Dysphagia after photodynamic therapy therefore may be related to underlying esophageal dysmotility and may not always be caused by stricture or underlying carcinoma.     

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.     

Frequency of Barrett's neoplasia after initial negative endoscopy with biopsy: a long-term histopathological follow-up study

BACKGROUND: Barrett's adenocarcinoma is being diagnosed increasingly. We examine possible differences between long segment and short-segment Barrett esophagus (LSBE and SSBE) in long-term follow-up on the basis of our histopathology registry. METHODS AND PATIENTS: All Barrett's esophagus patients diagnosed histologically between 1990 and 1995 (n = 1071) were selected. Long-term follow-up data from endoscopy with biopsy were sought on all patients without neoplasia on initial endoscopic biopsy (n = 1003). A total of 255 individuals (25.4 %) were regarded as drop-outs (201 lost and 54 without further endoscopy). Of the remaining 748 patients with follow up for more than 5 years, 315 had documented LSBE, 246 had SSBE, and 187 had no length of Barrett esophagus recorded (NLBE). RESULTS: In the study cases (male : female ratio 2.1 : 1, mean age +/- SD 60.9 +/- 14.2 years), the biopsy procedure was fully compliant with guidelines in only 32.5 %. Only 5 cases (0.6 %) had visible lesions reported on endoscopy, but all were negative for neoplasia. Over a mean follow-up of 78.2 +/- 35.6 months (range 0-240), 7 new cases of low grade intraepithelial neoplasia (LGIN) and 15 cancer cases developed, accounting for a yearly incidence of 0.2 % (LGIN) or 0.4 % (cancer) after an initial negative endoscopy. When the cases with initial diagnosis of neoplasia were included, this yearly incidence rose to 0.5 % (LGIN), 0.3 % (high grade intraepithelial neoplasia [HGIN]) or 1.7 % (cancer). Differences between SSBE and LSBE were only encountered for cancer incidence. CONCLUSION: The yearly incidence of Barrett esophagus cancer varies between 0.4 % and 1.7 %. Despite the limitations of this retrospective and pathology-based study, the observed risk of developing cancer in Barrett esophagus without neoplasia is comparable to that found in other studies, mainly from the US and the UK, and varies between 0.7 % and 1.0 % of yearly incidence.     

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.     

自体荧光联合窄带成像技术对 Barrett 食管上皮内瘤变的诊断价值

目的：评价自体荧光（AFI）联合窄带成像（NBI）技术对 Barrett食管上皮内瘤变的诊断价值。方法对50例患者自体荧光内镜诊断Barrett的74个可疑上皮内瘤变的病灶,进一步行窄带成像检查,观察黏膜微血管及小凹的改变,并于相应病变区取活检送病理检查。结果在AFI诊断74例可疑病灶中共有44例病灶病理确诊为高级别上皮内瘤变（HGIN）,30例病灶为假阳性。NBI对这44例病灶HGIN的诊断：确诊39例,可疑5例;在30例HGIN假阳性的病灶中,NBI假阳性为7例。两者的假阳性率由40.5%减少至14.9%。自体荧光内镜对Barrett食管HGIN诊断的阳性预测值为59.5%（44/74）,AFI联合NBI技术后诊断的阳性预测值为84.8%（39/46）。结论自体荧光联合NBI技术可提高Barrett食管高级别上皮内瘤变的检出率。     

胃食管反流病合并食管裂孔疝患者的临床特点分析

目的分析胃食管反流病(GERD)合并食管裂孔疝(HH)患者的临床特点及其危险因素。方法回顾性分析2018年1月-2019年3月在宁夏回族自治区人民医院消化内科诊断为GERD合并HH的40例患者并作为研究组,另外40例GERD未合并HH的患者为对照组,比较两组患者的基本临床资料、内镜分级、Barrett食管发生率。结果研究组患者的年龄、体重、吸烟史、糖尿病与对照组比较,差异均有统计学意义(P<0.05),两组性别、饮酒史和冠心病比较,差异均无统计学意义(P>0.05);研究组食管外症状较多见,内镜下分级仅有C级与对照组比较差异有统计学意义(P<0.05);A级、B级、D级两组差异无统计学意义(P>0.05);两组Barrett食管发生率比较,差异有统计学意义(P<0.05)。结论GERD合并HH与年龄、体重、吸烟史、糖尿病有关,且其会使Barrett食管发生率升高,积极防控可改变的因素对该类患者可能有一定的好处。     

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.