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Although the endoscopic submucosal dissection (ESD) has been established to be more efficacious in the treatment of superficial gastrointestinal neoplasia than the piecemeal resection, its use is still limited due to the concern about serious adverse events particularly in the west. Newer ESD knives have been developed that have been said to be safer than the first-generation devices. We aimed to report a Western single center experience regarding the initial safety and performance of ESD for superficial esophageal neoplasia treated with the Clutch Cutter (DP2618DT; Fujifilm Corporation, Tokyo, Japan). Our main outcome was safety in terms of bleeding or perforation. Secondary outcomes included en bloc resection and the R0 resection. Fourteen patients with superficial esophageal neoplasia underwent 15 ESDs using the Clutch Cutter. The mean age was 65 ± 16.7 years and 10 (71.4%) males. Eight (57%) patients had esophageal adenocarcinoma, 3 (21.4%) had high-grade dysplasia, 1 (7%) had nodular low-grade dysplasia, and 2 (14.3%) had squamous cell carcinoma. Mild anticipated intraprocedural bleeding was present with most procedures. However, no significant postoperative bleeding or perforation was encountered. One patient had mild chest pain postprocedure. En bloc resection was achieved in all lesions 100%. Histological R0 was achieved in 5/12 lesions (41.6%). The mean length of the resected area was 24.8 ± 13 mm (IQR: 17-30 mm). All patients were safely discharged home after overnight observation. In conclusion, this is the largest series of esophageal ESD using the multimodal Clutch Cutter in the United States; we found that the device effectively achieved en bloc resection of superficial esophageal neoplasia without significant adverse events. The use of the Clutch Cutter should be considered as one option to minimize adverse events during ESD in the Western population.

Summary Barrett's esophagus (BE) with high-grade dysplasia (HGD) defines a group of individuals at high risk of progression to esophageal adenocarcinoma (EA). Fluorescence in situ hybridization (FISH) has been shown to be useful for the detection of dysplasia and EA in endoscopic brushing specimens from BE patients. The aim of this study was to determine whether FISH in combination with histological findings would further identify more rapid progressors to EA. This is a retrospective cohort study of high-risk patients, having a history of biopsy-confirmed HGD without EA, with an endoscopic brushing specimen analyzed by FISH while undergoing endoscopic surveillance and treatment between April 2003 and October 2010. Brushing specimens were assessed by FISH probes targeting 8q24 (MYC), 9p21 (CDKN2A), 17q12 (ERBB2), and 20q13 (ZNF217) and evaluated for the presence of polysomy, defined as multiple chromosomal gains (displaying ≥ 3 signals for ≥ 2 probes). Specimens containing ≥ 4 cells exhibiting polysomy were considered polysomic. HGD was confirmed by at least two experienced gastrointestinal pathologists. Of 245 patients in this study, 93 (38.0%) had a polysomic FISH result and 152 (62.0%) had a non-polysomic FISH result. Median follow-up was 3.6 years (interquartile range [IQR] 2–5 years). Patients with a polysomic FISH result had a significantly higher risk of developing EA within 2 years (14.2%) compared with patients with a non-polysomic FISH result (1.4%, P < 0.001). These findings suggest that a polysomic FISH result in BE patients with simultaneous HGD identifies patients at a higher risk for developing EA compared with those with non-polysomy.

Background Endoscopic mucosal resection (EMR) can be performed en-bloc in Barrett's esophagus (BE) lesions that are ≤2 cm in size. The true size of a BE lesion may be underestimated under white light endoscopy, limiting the rate of en-bloc resection. Volumetric laser endomicroscopy (VLE) provides high-resolution cross-sectional imaging of BE. A greater number of VLE glands are associated with BE dysplasia and may help predict lesion size. The aim of this study was to determine the association between VLE gland count and outcome of resection. Methods EMR specimens from patients with a history of dysplastic BE were imaged with VLE. EMRs performed on BE lesions ≤2cm in size with intent at en-bloc resection were included. Manual quantification of epithelial glands was performed in blinded fashion. Image visualization enhancement software was used to quantify the surface area occupied by epithelial glands on en-face VLE. Histologic en-bloc (R0) and incomplete (R1) resection of the targeted lesion was defined by the absence and presence of dysplasia and/or cancer at the specimen margins respectively. Results The study sample consisted of 37 EMRs from 31 patients. The mean (SD) size of EMRs was 1.04 (0.37) cm. Pathology showed low-grade dysplasia (N = 12), high-grade dysplasia (N = 19), and intramucosal cancer (N = 6). The en-bloc resection rate was 37.8% (R0: N = 14; R1: N = 23). The mean (SD) number of epithelial glands was 13.0 (6.7) and 28.8 (23.9) for R0 and R1 specimens, respectively, with a statistically significant mean difference of 15.8 glands (95% CI: 2–29, P = 0.02) between the two groups. A gland count of 28 or higher per EMR specimen predicted R1 with 100% sensitivity and 39% specificity (ROC: 0.69). The mean (SD) surface area occupied by epithelial glands in R0 and R1 specimens was 0.98 (1.1) mm2 and 2.3 (2.4) mm2, respectively. There was strong correlation between manual gland counts and epithelial gland surface area (R2: 0.81, P Conclusion A higher number of VLE glands in EMR specimens is associated with a lower en-bloc resection rate suggesting that white-light endoscopy underestimates lesion size and that VLE may have a potential role in lesion margin assessment. Disclosure All authors have declared no conflicts of interest.

Background Post-surgical complications such as leaks are the source of considerable morbidity and mortality. Success of conservative interventions is highly variable. Recurrence after surgical repair is also not uncommon. Our aim was to develop novel endoscopic strategies to maximize negative intracavitary pressure to manage leaks in cases where conventional management either failed or were not feasible. Methods We have used transluminal locking loop drains with low intermittent suction in the management of non-healing leaks in various areas. An example presented here illustrates this concept where a 68-year-old male patient underwent paraesophageal hernia repair with Nissen fundoplication. Patient presented 3 weeks later with fistula leading to a 13 cm meditational abscess. Patient developed right hemiparesis requiring tissue plasminogen activator (tPA). Post-tPA patient developed hemoptysis and hematemesis requiring emergency intubation. The defect in the esophagus was 6–8 mm. Endoscopic repair with stitching or clipping would have left a large undrained cavity with a potential to expand. Endoscopic repair with transcutaneous drain placement was challenging due to recent tPA and a difficult location. Moreover there was potential to develop esophago- pleural- broncho- cutaneous fistula. Endoscopic vacuum therapy was felt to be a suboptimal choice. Patient was high-risk surgical candidate as it would have required radical surgery in the setting of tPA.Upper endoscopy was performed and the cavity was debrided. No direct communication with bronchopulmonary tree noted. A transnasal guidewire assisted 16 Fr, 60 cm locking loop drain was placed and connected to low intermittent suction that was switched to bulb based suction. Results The output from naso-cavity drain decreased nearly 100 cc per day in the first 5 days and the size reduced by 30, 50 and 80% by day 5, 9 and 12 respectively. Near complete elimination of the cavity was observed on day 15. Esophagogram showed complete resolution of the leak and computerized tomography revealed no residual cavity Conclusion Developing transluminal endoscopic strategies to maximize negative intracavitary pressure helps expedite the healing of resistant postsurgical leaks. This technique avoids the need for frequent drain changes that remains a challenge for vacuum therapy. Disclosure All authors have declared no conflicts of interest.

Barrett's esophagus (BE) is the strongest risk factor for the development of esophageal adenocarcinoma. However, the risk of cancer progression is difficult to ascertain in individuals, as a significant number of patients with BE do not necessarily progress to esophageal adenocarcinoma. There are several issues with the current strategy of using dysplasia as a marker of disease progression. It is subject to sampling error during biopsy acquisition and interobserver variability among gastrointestinal pathologists. Ideal biomarkers with high sensitivity and specificity are needed to accurately detect high-risk BE patients for early intervention and appropriate cost-effective surveillance. To date, there are no available molecular tests in routine clinical practice despite known genetic and epigenetic aberrations in the Barrett's epithelium. In this review, we present potential biomarkers for the prediction of malignant progression in BE. These include markers of genomic instability, tumor suppressor loci abnormalities, epigenetic changes, proliferation markers, cell cycle predictors, and immunohistochemical markers. Further work in translating biomarkers for routine clinical use may eventually lead to accurate risk stratification.

SUMMARY The management of high-grade dysplasia in Barrett's esophagus has clearly changed over recent years. The risk of cancer development is still substantial, with about one in three patients developing cancer, but a number of patients do not develop cancer. The nature of high-grade dysplasia has also been genetically elucidated with more evidence of chromosomal instability being present at this stage than previously thought. Therapy of the condition has evolved more toward endoscopic therapy, given the good results of radio-frequency ablation and photodynamic therapy in eliminating dysplasia and decreasing cancer development in randomized controlled trial. The best candidates for treatment include compliant patients that have relatively short segments of Barrett's esophagus, an anatomically straight segment, lack of nodularity, and an intact p16. However, even with excellent long-term results similar to surgical resection, the risk of recurrence is present in over 14% of patients, which indicates that there will be a need to continue surveillance endoscopy in these patients.

Markedly increased esophageal eosinophils are associated with allergy- or reflux-based eosinophilic esophagitis. Other known disorders that cause this entity are unusual. To characterize the clinical, endoscopic, and histological findings of patients who develop marked esophageal eosinophilic infiltration after ablative therapy for Barrett's dysplasia. All patients who underwent endoscopic ablation of Barrett's esophagus between 1991 and 2009 with photodynamic therapy or radio frequency were screened for a pathologic descriptor of 'eosinophils' on biopsy. Patients whose biopsies demonstrated >15 eosinophils per high power (HPF) field in squamous epithelium after ablation were reviewed and included in the study group. Thirteen of 385 (3.4%) patients underwent ablation for Barrett's esophagus and subsequently had large numbers of intraepithelial eosinophils. All patients had long segment Barrett's (mean 8.0 cm) with low- or high-grade dysplasia or adenocarcinoma. All had undergone photodynamic therapy as their form of ablation. No patients had typical symptoms or endoscopic findings of eosinophilic esophagitis. Eleven patients were on proton pump inhibitors. The time between ablation and onset of esophageal eosinophilia ranged from 83 to 692 days. Intraepithelial eosinophil counts ranged from 30 to 150/HPF (mean 90). The majority of cases showed eosinophilic degranulation, spongiosis, increased papillary height, and basal zone thickening. The natural history of esophageal eosinophilia was variable after ablation, persisting consistently or sporadically on biopsy for up to 6 years. Ablation for Barrett's dysplasia can be followed rarely by eosinophil infiltrates with a histological resemblance to allergy-based eosinophilic esophagitis, but lacking dysphagia. The pathophysiology is unknown.

SUMMARY Granular cell tumors (GCT) are uncommon neoplasms. There is controversy regarding the endoscopic diagnosis and treatment of esophageal GCT. We studied the endoscopic diagnosis and management of esophageal GCT among 23 patients identified in a single-institution pathology database. Medical records, pathology, and endoscopic images were reviewed. All patients underwent endoscopy and endoscopic ultrasonography (EUS), and endoscopic resection was performed in 10 patients. Seven of 23 patients had more than one esophageal GCT. Only six lesions exhibited a classic yellow discoloration. Among patients with a single GCT, three, four, and nine lesions were located in the proximal, middle, and distal esophagus, respectively. EUS showed hypoechoic, smooth-edged lesions usually confined to deep mucosa and submucosa. Standard forceps biopsy was diagnostic in 19 of 23 patients (83%). Ten GCT ≤ 10 mm in diameter underwent successful endoscopic mucosal resection without complication. The endoscopic appearance, location, and number of esophageal GCT are highly variable. Histological proof is still necessary for the differential diagnosis of this rare neoplasm. Endoscopic forceps biopsy is usually diagnostic. Endoscopic resection appears safe and effective in selected cases with lesions ≤ 10 mm.

Background The neo-squamous epithelium that replaces columnar epithelium after successful endoscopic ablation of Barrett's esophagus (BE) has not been fully characterized in regard to its structural and functional integrity. Intercellular space is a surrogate marker for epithelial structural integrity and mucosal impedance (MI) is a surrogate for transepithelial resistance and thus epithelial functional integrity. Impairment of the structural and functional integrity may influence recurrence following successful ablation. We aimed to measure the esophageal epithelial intercellular space diameter and MI in the neo-squamous and normal squamous epithelium of patients who underwent successful radiofrequency ablation for dysplastic BE. Methods Forty patients with complete remission of intestinal metaplasia (CRIM) (defined as two negative surveillance endoscopies for intestinal metaplasia) were prospectively recruited. Patients were excluded if they had endoscopic evidence of esophagitis. MI measurements were taken at 1 cm above the GE junction and 2 cm above the prior BE segment (targeting uninvolved squamous epithelium), using a novel through the scope MI probe. Endoscopic biopsies were also taken at these corresponding sites to assess intercellular space diameter using transmission electron microscopy (TEM) using standard techniques. Results 80% of patients were male with a mean age of 69 years. Mean follow since achieving CRIM was 30 months. 39 patients underwent RFA for dysplasia. The mean intercellular space diameter was higher in the neo-squamous epithelium (1.01 μm) when compared to the untreated native squamous epithelium (0.96 μm) [Difference of 0.056 μm, 95% CI of -0.036 to 0.148, P = 0.228]. The mean MI was significantly lower in the neosquamous epithelium (4001.3 Ω) when compared to the untreated native epithelium (5168.1 Ω) [Difference of 1166.7 Ω, 95% CI 418.8 to 1914.6, P = 0.003]. Conclusion Neo-squamous epithelium that replaces BE epithelium following successful endoscopic therapy for BE appears to be functionally and likely structurally deficient with regards to acid reflux barrier function, when compared to native squamous esophageal epithelium. This impairment may be associated with recurrence following successful ablation. Disclosure All authors have declared no conflicts of interest.