Short-segment Barrett's Esophagus Research Articles

Early metal stent insertion fails to prevent stricturing after single-stage complete Barrett's excision for high-grade dysplasia and early cancer

Barrett's esophagus with high-grade dysplasia (HGD) or intramucosal adenocarcinoma (IMC) can be effectively treated by single-session EMR, resulting in complete Barrett's excision (CBE). CBE provides accurate histology for staging and clinical confirmation of neoplasia eradication but is limited by a high risk of esophageal stricture formation. To evaluate the effectiveness of prophylactic temporary esophageal stenting to prevent post-CBE stricture formation. Single-center, investigator-initiated feasibility study. Circumferential, short-segment Barrett's esophagus (≤C3≤M5) with HGD or IMC. Single-stage CBE and insertion of a fully covered metal esophageal stent at 10 days that was removed at 8 weeks. Patients were followed for a minimum of 2 surveillance endoscopies. Symptomatic esophageal stricture formation. At the end of the follow-up period, 8 patients (57.1%) required esophageal dilation for symptomatic CBE-related (n= 7) or stent-related (n= 4) strictures. A median of 3 surveillance endoscopies were performed over a median endoscopic follow-up of 17 months (range 4-25 months). Single-stage CBE successfully eliminated Barrett's intestinal metaplasia and neoplasia in 71.4% and 92.9% of patients, respectively. Four patients were admitted to the hospital, and 4 patients had early stent removal because of pain or dysphagia. Single-center feasibility study. In a prospective study evaluating prophylactic esophageal stent insertion after single-stage CBE, esophageal strictures formed in more than of half the study cohort, and stents were associated with significant morbidity. An alternative method to reduce stricture formation is required. ( NCT01554280.).

Neoplastic progression in short-segment Barrett's oesophagus is associated with impairment of chemical clearance, but not inadequate acid suppression by proton pump inhibitor therapy.

Pathophysiological mechanisms associated with neoplastic progression in patients with short-segment Barrett's oesophagus (SSBO), who represent the vast majority of the Barrett population, have not been defined. To evaluate pathophysiological characteristics of patients with SSBO and dysplasia detected at 3-year surveillance endoscopy (incident dysplasia). Patients with SSBO underwent impedance-pH monitoring during heartburn-suppressing PPI therapy. Fifteen patients (12 males, median age 62 years) with incident dysplasia and 50 patients (43 males, median age 59 years) without dysplasia were compared. Impedance-pH parameters, including chemical clearance assessed by the post-reflux swallow-induced peristaltic wave (PSPW) index, were evaluated. All patients declared persisting heartburn suppression on maintenance PPI therapy at 3-year follow-up, 58/65 (89%) with standard dosages. The median gastric and oesophageal acid exposure time (GAET and OAET) did not differ between patients with and without incident dysplasia at the time of surveillance (36% and 0.6% vs. 33% and 0.5%) or index endoscopy (33% and 0.3% vs. 41% and 0.5%) (P > 0.05). Contrastingly, the median PSPW index was significantly lower in patients with than in patients without incident dysplasia at the time of surveillance (15%, vs. 32%) and index endoscopy (12% vs. 30%) (P = 0.001). The PSPW index, the GAET and the OAET did not vary over time (P > 0.05). A PSPW index <26% was predictive of incident dysplasia with a 75% accuracy. Neoplastic progression in SSBO is associated with impairment of chemical clearance, but not inadequate acid suppression by PPI therapy. Neoplastic progression in SSBO can be predicted by a low PSPW index.

What is the long-term risk of short segment Barrett's esophagus?

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Antireflux surgery for dysplastic Barrett.

Barrett's esophagus (BE) is the result of continuous injury of the esophageal mucosa by gastric refluxate. This condition can progress to low-grade (LGD) and high-grade dysplasia (HGD) and eventually to adenocarcinoma. While excellent results are reported in terms of reflux and symptom control in patients with BE undergoing antireflux surgery (ARS), the impact of a fundoplication on progression and regression of dysplasia is debated. The aim of this article is to review the effects of ARS on regression and progression of LGD to HGD or cancer in patients with dysplastic BE. A review of the literature in PubMed/Medline electronic databases has been performed. ARS might decrease but not eliminate the risk of progression to dysplasia or cancer in BE patients. ARS may promote regression of dysplastic BE only in short-segment BE, but not in long-segment BE. Modulation of gene expression is involved in the genesis and reversion of short-segment intestinal metaplasia after ARS. Close and long-term surveillance by 24-hour pH monitoring and upper endoscopy is recommended in BE patients who undergo ARS to identify postoperative pathological reflux, and to early detect dysplasia or even adenocarcinoma. Further studies are requested to assess the molecular effects of ARS in dysplastic BE.

Symptoms and Endoscopic Features at Barrett's Esophagus Diagnosis: Implications for Neoplastic Progression Risk

Risk stratification of Barrett's esophagus (BE) patients based on clinical and endoscopic features may help to optimize surveillance practice for esophageal adenocarcinoma (EAC) development. The aim of this study was to investigate patient symptoms and endoscopic features at index endoscopy and risk of neoplastic progression in a large population-based cohort of BE patients. A retrospective review of hospital records relating to incident BE diagnosis was conducted in a subset of patients with specialized intestinal metaplasia from the Northern Ireland BE register. Patients were matched to the Northern Ireland Cancer Registry to identify progressors to EAC or esophageal high-grade dysplasia (HGD). Cox proportional hazards models were applied to evaluate the association between endoscopic features, symptoms, and neoplastic progression risk. During 27,997 person-years of follow-up, 128 of 3,148 BE patients progressed to develop HGD/EAC. Ulceration within the Barrett's segment, but not elsewhere in the esophagus, was associated with an increased risk of progression (hazard ratio (HR) 1.72; 95% confidence interval (CI): 1.08-2.76). Long-segment BE carried a significant sevenfold increased risk of progression compared with short-segment BE; none of the latter group developed EAC during the study period. Conversely, the absence of reflux symptoms was associated with an increased risk of cancer progression (HR 1.61; 95% CI: 1.05-2.46). BE patients presenting with a long-segment BE or Barrett's ulcer have an increased risk of progressing to HGD/EAC and should be considered for more intense surveillance. The absence of reflux symptoms at BE diagnosis is not associated with a reduced risk of malignant progression, and may carry an increased risk of progression.

Barrett's Esophagus and Intestinal Metaplasia of Gastric Cardia: Prevalence, Clinical, Endoscopic and Histological Features

Over the past few decades, the incidence of adenocarcinomas of the gastroesophageal junction has rapidly increased. Barrett's esophagus is a risk factor for esophageal adenocarcinoma, but the role of intestinal metaplasia of the gastric cardia as a precursor in cardia-related cancer is controversial. The aims of the present study were to examine the prevalence of intestinal metaplasia in the gastroesophageal junction and to evaluate the clinical, endoscopical and histological features of patients with intestinal metaplasia in the gastric cardia and patients with Barrett's esophagus. 286 consecutive patients undergoing gastroduodenoscopy were enrolled in a prospective study. Biopsy specimens were performed in the distal esophagus, squamocolumnar junction, gastric cardia, gastric corpus and antrum. We identified 44 patients (15.3%) with intestinal metaplasia in biopsies from gastric cardia and 24 patients (8.3%) with Barrett's esophagus. Cardia intestinal metaplasia was significantly associated with older age (p=0.03), with intestinal metaplasia in the antrum (p=0.017) and H. pylori infection (p<0.0001). Severe chronic cardia inflammation increased the presence of cardia intestinal metaplasia 6.2 fold (OR=6.288; p<0.0001). Patients with Barrett's esophagus were predominantly men. Barrett's esophagus presence significantly correlated with reflux symptoms(p<0.0001), endoscopic esophagitis (p<0.0001) and hiatal hernia >2 cm (p=0.002). No patient had dysplasia in the gastroesophageal region. Presence of intestinal metaplasia at the gastroesophageal region correlated with reflux symptoms and endoscopic signs of reflux disease in patients with Barrett's esophagus and with H.pylori infection and distal intestinal metaplasia in patients with cardia intestinal metaplasia.

Clinical outcomes of endoscopic submucosal dissection for superficial Barrett's adenocarcinoma

Advances in diagnostic techniques have allowed early stage detection of superficial Barrett's adenocarcinoma (SBA) as well as resection by endoscopic submucosal dissection (ESD). Few reports exist, however, on the safety and efficacy of ESD for SBA. To analyze outcomes of ESD for SBA in relation to clinicopathological features of the lesions. Retrospective study. University hospital. Twenty-three patients (21 men, 2 women; mean age, 63 years) with 26 SBAs. We examined outcomes of ESD in relation to the clinicopathological features of SBAs. The main outcomes assessed were en bloc resection rate, operation time, adverse event rates, additional resection rate, and time between ESD and any recurrence. Twenty lesions (87%) derived from short-segment Barrett's esophagus, and 3 lesions (13%) derived from long-segment Barrett's esophagus. The majority of SBAs (54%) were located in the 0 to 3 o'clock circumferential quadrant. Median tumor size was 15 mm (range 5-60 mm). Macroscopic types were flat elevated (n = 13, 50%), depressed (n = 12, 46%), and protruded (n = 1, 4%). The SBAs appeared red (n = 23, 88%) or normally pale (n = 3, 12%). Under magnifying narrow-band imaging, all SBAs showed an irregular mucosal pattern and an irregular vascular pattern. The endoscopic en bloc resection rate was 100% (26/26), and the pathological en bloc resection rate was 85% (22/26). The median procedure time was 95 minutes (range, 30-210 minutes). Delayed bleeding occurred in 1 case, but there was no perforation. The SBAs were of the differentiated type (n = 25, 96%) or poorly differentiated type (n = 1, 4%). The tumor had invaded the superficial muscularis mucosa (n = 3, 12%), lamina propria mucosa (n = 5, 19%, deep muscularis mucosa (n = 9, 34%), SM1 (n = 3, 12%), and SM2 (n = 6, 23%). Additional surgical resection after ESD was performed in 9 cases, and there were no residual tumors, but 1 lymph node metastasis was found. There were no recurrent tumors; however, 1 metachronous adenocarcinoma was diagnosed 42 months after ESD. Single-center, retrospective study. ESD appears to be a safe and effective treatment strategy for early stage SBA.

Physicians' Opinion on Asymptomatic Reflux Esophagitis and Short Segment Barrett's Esophagus

Physicians' Opinion on Asymptomatic Reflux Esophagitis and Short Segment Barrett's Esophagus

Impairment of secondary peristalsis in Barrett’s esophagus by transnasal endoscopy-based testing

To investigate dysfunctions in esophageal peristalsis and sensation in patients with Barrett's esophagus following acid infusion using endoscopy-based testing. First, physiological saline was infused into the esophagus of five healthy subjects, at a rate of 10 mL/min for 10 min, followed by infusion of HCl. Esophageal contractions were analyzed to determine whether the contractions observed by endoscopy and ultrasonography corresponded to the esophageal peristaltic waves diagnosed by manometry. Next, using nasal endoscopy, esophageal sensations and contractions were investigated in patients with, as well as controls without, Barrett's esophagus using the same infusion protocol. All except one of the propulsive contractions identified endoscopically were recorded as secondary peristaltic waves by manometry. Patients with long segment Barrett's esophagus (LSBE) tended to have a shorter lag time than the control group, although the difference did not reach statistical significance (88 ± 54 s vs 162 ± 150 s respectively, P = 0.14). Furthermore, patients with LSBE had significantly fewer secondary contractions following the infusion of both saline and HCl than did either the control group or patients with short segment Barrett's esophagus (4.1 ± 1.2 vs 8.0 ± 2.8, P < 0.001 and 7.3 ± 3.2, P < 0.01, respectively, following saline infusion; 5.3 ± 1.2 vs 8.4 ± 2.4 and 8.1 ± 2.9 respectively, P < 0.01 for both, following infusion of HCl). Using nasal endoscopy and a simple acid-perfusion study, we were able to demonstrate disorders in secondary peristalsis in patients with LSBE.

Risk factors associated with Barrett's epithelial dysplasia.

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

Recent advances in oesophageal diseases.

Recent advances in oesophageal diseases.

Barrett Esophagus in Asia: Same Disease with Different Pattern

Barrett esophagus (BE) is considered to develop as a result of chronic gastroesophageal reflux disease (GERD) and to predispose to esophageal adenocarcinoma (EAC). However, the disease pattern of BE in Asia differs from that observed in the West. For example, in the West, the prevalence rates of BE and EAC have progressively increased, whereas although the prevalence rate of GERD is increasing in Asia, the prevalence rates of BE and EAC have remained low in most Asian countries. GERD, hiatal hernia, old age, male sex, abdominal obesity (visceral obesity), smoking, alcohol consumption, and kyphosis are known risk factors for BE in Asia, and most Asian patients have short-segment BE. Helicobacter pylori infection is more prevalent in Asia than in the West. We suggest larger studies with a prospective design be conducted to elaborate further the different patterns of BE in Asia.

Circulating Inflammatory Cytokines and Adipokines Are Associated With Increased Risk of Barrett's Esophagus: A Case–Control Study

Obesity is associated with Barrett's esophagus (BE) and with changes in circulating levels of adipokines (leptin and adiponectin) and cytokines. Although studies have reported that adipokines and inflammatory cytokines are necessary for the development of BE, their role is controversial.We performed a case-control study; cases (n = 141) were patients who underwent esophagogastroduodenoscopy and were found to have BE, which was based on endoscopy and histology, and controls (n = 139) were primary care patients eligible for screening colonoscopies who agreed to undergo esophagogastroduodenoscopy. We examined the association between BE and circulating levels of adipokines and cytokines (interleukin [IL]-1β, IL-6, IL-8, IL-10, and IL-12p70; tumor necrosis factor-α; and interferon-γ). Cases and controls were compared by calculating odds ratios (ORs) and 95% confidence intervals (CIs) and using unadjusted and multiple logistic regression, adjusting for age, sex, race, waist-hip ratio, use of proton pump inhibitors and nonsteroidal anti-inflammatory drugs, and Helicobacter pylori infection.The adjusted ORs for BE were 2.62 (95% CI, 1.0-6.8), 5.18 (95% CI, 1.7-15.7), and 8.02 (95% CI, 2.79-23.07) for the highest quintile vs the lowest quintile of levels of IL-12p70, IL-8, and leptin, respectively, but the OR was not significant for IL-6 (2.39; 95% CI, 0.84-6.79). The adjusted OR for BE was 0.14 for highest quintile of IL-10 compared with lowest quintile (95% CI, 0.05-0.35) and 0.03 for IL-1β ≥ median vs none detected (95% CI, 0.006-0.13). Higher levels of IL-8 and leptin and lower levels of IL-10 and IL-1β were associated with the presence of long-segment (≥3 cm) and short-segment BE. There were no differences between cases and controls in levels of interferon-γ, tumor necrosis factor-α, adiponectin, or insulin.BE is associated with circulating inflammatory cytokines and leptin and low levels of anti-inflammatory cytokines. These findings could partly explain the effect of obesity on BE.

Carcinogenesis of Barrett's esophagus: a review of the clinical literature.

Barrett's esophagus (BE) is a premalignant condition of esophageal adenocarcinoma (EAC). Although the incidence of BE has risen rapidly in the West, it is rare in Asia despite a recent increase in the prevalence of gastroesophageal reflux disease. Controversies over the definition of BE are presented because most cases show short-segment BE, especially ultra-short BE, in Asia. Here we review possible risk factors for the development of EAC, particularly possible roles of ethnicity, specialized intestinal metaplasia (SIM), BE length, and environmental factors, such as Helicobacter pylori infection and obesity. Additionally, we summarize recent studies on the effect of chemoprevention including proton pump inhibitors, nonsteroidal anti-inflammatory drugs or aspirin in order to reduce the risk of neoplastic progression in BE patients. Although substantial knowledge of risk factors of dysplasia/EAC in BE is shown, the risk for neoplastic development may be influenced by geographic variation, study population, the presence or absence of SIM or dysplasia at baseline, and the small number of BE patients investigated. Recently, the efficiency of surveillance for BE patients has been discussed from the standpoint of cost-effectiveness. It may be too difficult to draw conclusions because no randomized clinical trials of BE surveillance have been performed.

The Dose of Omeprazole Required to Achieve Adequate Intraesophageal Acid Suppression in Patients with Gastroesophageal Junction Specialized Intestinal Metaplasia and Barrett’s Esophagus

The mainstay of medical therapy for Barrett's esophagus is normalization of esophageal acid exposure with proton pump inhibitors (PPIs). However, the optimal dose and whether once daily or twice daily is required for acid suppression is unknown. The purpose of this study was to assess whether adequate intra-esophageal acid suppression could be achieved with once daily versus twice daily omeprazole in patients with gastroesophageal specialized intestinal metaplasia (GEJSIM), short-segment (SSBE) and long-segment Barrett's esophagus (LSBE). Patients with GEJSIM and Barrett's esophagus underwent upper endoscopy with 48-h wireless pH capsule while on once daily 20 mg omeprazole for at least 1 week. If intra-esophageal acid was not adequately controlled, defined as pH value <4 for greater than 4.2 % of the time during the second 24-h period, omeprazole was increased to twice daily for 1 week and upper endoscopy with wireless pH capsule was repeated. A total of 36 patients completed the study (10 patients had GEJSIM, 16 patients had SSBE, and 10 patients had LSBE). Normalization of intraesophageal pH was achieved in 28 patients (78 %) with once daily PPI and eight patients required twice daily PPI. There was no significant difference between the three groups in the proportion of patients requiring high dose PPI (GEJSIM 10 %, SSBE 25 %, LSBE 30 %, p = 0.526). The majority of patients with Barrett's esophagus were controlled with once daily low dose PPI and only a minority required twice daily dosing, regardless of the length of Barrett's mucosa.

SYMPTOMS AND ENDOSCOPIC FEATURES AT BARRETT'S OESOPHAGUS DIAGNOSIS: IMPLICATIONS FOR NEOPLASTIC PROGRESSION RISK

IntroductionRisk stratification of Barrett's oesophagus (BO) patients based on clinical and endoscopic features may help to optimise surveillance for early detection/prevention of oesophageal adenocarcinoma (OAC) development.Aims/BackgroundThe aim of this study...

Oxidative DNA Damage in Barrett Mucosa: Correlation with Telomeric Dysfunction and p53 Mutation

Barrett esophagus develops in a scenario of chronic inflammation, linked to free radical formation and oxidative DNA damage. Eight-hydroxydeoxyguanosine, the main oxidative DNA adduct, is partially repaired by a glycosylase (OGG1) whose polymorphism is associated to a reduced repair capacity. Telomeres are particularly prone to oxidative damage, which leads to shortening and cell senescence, while elongation, by telomerase activity, is linked to cell immortalization and cancer. Limited data are available on this point with respect to Barrett esophagus. This study aimed to evaluate the link among 8-hydroxydeoxyguanosine, OGG1 polymorphism, telomerase activity, telomere length, and p53 mutation in Barrett progression. Forty consecutive patients with short- and long-segment Barrett esophagus and 20 controls with gastroesophageal reflux disease without Barrett esophagus were recruited. Analysis of biopsy samples was undertaken to study 8-hydroxydeoxyguanosine levels, OGG1 polymorphism, telomerase activity, and telomere length. Serum samples were obtained for p53 mutation. Controls had significantly lower levels of 8-hydroxydeoxyguanosine and telomerase activity, with normal telomere length and no p53 mutation. In short-segment Barrett esophagus, 8-hydroxydeoxyguanosine levels were higher and telomeres underwent significant shortening, with stimulation of telomerase activity but no p53 mutations. In long-segment Barrett esophagus, 8-hydroxydeoxyguanosine reached maximal levels, with telomere elongation, and 42 % of the patients showed p53 mutation. In Barrett patients, with disease progression, oxidative DNA damage accumulates, causing telomere instability, telomerase activation, and, in a late phase, mutations in the p53 gene, thus abrogating its activity as the checkpoint of proliferation and apoptosis, and facilitating progression to cancer.

52 Clinical Efficacy of Endoscopic Submucosal Dissection for Adenocarcinomas of the Esophagogastric Junction

Although endoscopic submucosal dissection (ESD) has been widely used for treating superficial gastrointestinal cancers, only a few reports have been published on ESD for adenocarcinomas of the esophagogastric junction (EGJ). In Japan, most cases of Barrett's adenocarcinoma (BA) arising from the short-segment Barrett's esophagus are difficult to distinguish from cases of non-Barrett's adenocarcinoma (NB) arising from the cardiac epithelium. In this study, the accurate diagnosis of BA and NB were confirmed pathologically after performing ESD of adenocarcinomas of the EGJ.

Magnifying endoscopy with narrow‐band imaging findings in the diagnosis of Barrett's esophageal adenocarcinoma spreading below squamous epithelium

It has been described that most cases of Barrett's esophageal adenocarcinoma in Japan are cases of Barrett's esophageal adenocarcinoma on a background of short-segment Barrett's esophagus, frequently occurring rostrad to Barrett's epithelium, adjacent to the squamous epithelium of the right wall of the esophagogastric junction. Barrett's esophageal adenocarcinoma may spread below the squamous epithelium when the tumor is situated adjacent to the squamocolumnar junction, so that it is usually difficult to diagnose its presence and extent by conventional endoscopy alone. We have noted that the spread of Barrett's esophageal adenocarcinoma below the squamous epithelium is recognizable as annular vascular formations (AVF) by magnifying endoscopy with narrow-band imaging (ME-NBI), and have verified it by 3-D stereo-reconstruction using serial sections from a specimen of the same lesion. When horizontal cross-sections of the tissue were viewed from the surface, AVF emerged at a depth of approximately 100 μm from the surface and disappeared at a depth of approximately 300 μm. Therefore, it would be presumed to be difficult to visualize the characteristic structural features by ME-NBI if the carcinomatous glandular ducts were situated deeper than approximately 300 μm underneath a thick layer of squamous epithelium. Thickness of the overlying squamous epithelium may be a limiting factor for whether or not the characteristic structural features can be detected.

Adenocarcinoma arising from short‐segment Barrett's esophagus in a young man

We report herein a case of adenocarcinoma arising from short-segment Barrett's esophagus (SSBE) in a 36-year-old man. An elevated tumor was found at the esophagogastric junction, and a histological evaluation of the biopsy specimen led to a diagnosis of adenocarcinoma. The tumor was found to be confined to the mucosa surrounding the SSBE, and endoscopic submucosal dissection was done without complications. Histological examination of the resected specimen showed that the adenocarcinoma had also invaded the muscularis mucosae and provided evidence of lymphovascular invasion. Additional surgical resection and regional lymph node dissection were therefore carried out; however, no lymph node metastasis was found. Adenocarcinoma arising from Barrett's mucosa is rare in young patients, especially in Japan, and this case is therefore particularly noteworthy.