Gastric inlet patches are often incidental, but can also be a treatable cause of laryngo-esophageal symptoms.

We retrospectively reviewed all patients whose gastric inlet patches were diagnosed following assessment for laryngopharyngeal and swallowing symptoms. Improvement following Argon Plasma Coagulation (APC) was assessed using Minimum Clinically-Important Difference methodology combining voice, throat, and swallowing domains. Correlations between APC response and measures of reflux and mucosal barrier integrity, measured during 24-h pH-impedance manometry, were obtained. Proximal and Distal Mean Nocturnal Baseline Impedance (MNBI) values were separately calculated and the novel variable of Mucosal Impedance Gradient was derived as [((Distal MNBI-Proximal MNBI)/((Distal MNBI + Proximal MMBI)/2)) x 100].

Inlet patches were detected in 57 of 651 patients who had Transnasal Panendoscopy (8.7 ± 2.2%). There were 34 males. Mean age was 58 years. Mean duration of symptoms was 2 years. The commonest symptoms were hoarseness (n = 33), throat symptoms (n = 24), and dysphagia (n = 21), respectively. APC was used to ablate patches in 34 patients. Treatment response was 71% at a mean followup of 5.5 months. MIG > - 25% predicted response to APC, with area under the receiver operating characteristic curve of 0.875 (Sensitivity = 81%; Specificity = 100%; p < 0.0001).

Gastric inlet patches are common and under-recognized. They can cause protracted pharyngo-esophageal symptoms. Patch ablation is an effective treatment for carefully selected patients. Optimal patient selection requires multidisciplinary teamwork. Mucosal Impedance Gradient could further refine patient selection.

Intestinal metaplasia (IM) in the esophagus is a potentially premalignant mucosal change. The aim of this study was to compare the frequency of IM detection during upper endoscopy by forceps biopsy sampling (FB) versus wide-area transepithelial sampling (WATS) brush.

Patients presenting for upper endoscopy for foregut symptoms or surveillance of Barrett's esophagus (BE) at 9 centers in the United States were randomized to either FB or WATS.

Of 1002 patients, FB was done in 505 and WATS in 497. The overall frequency of finding IM was 21% and was similar with FB (19.6%) and WATS (22.7%, P = .2). Low-grade dysplasia was found in 8 patients. No patient had high-grade dysplasia. There was no difference in detection of dysplasia between FB and WATS. In patients with no history of IM, WATS found significantly more IM compared with FB when a columnar-lined esophagus (CLE) was present (32.4% with WATS vs 15.2% with FB, P = .004). In 184 patients with known BE, FB and WATS found IM with similar frequency (38.5% FB vs 41.9% WATS, P = .6) with no difference in short- or long-segment BE.

Overall, FB and WATS detected a similar frequency of IM and dysplasia. WATS was twice as likely as FB to find IM in patients without a history of BE who had CLE on endoscopy. In patients with known BE, WATS and FB showed IM and dysplasia with similar frequency. These findings suggest that WATS can be used instead of FB with similar or improved efficacy at detecting IM and dysplasia. (Clinical trial registration number: NCT03859557.).

Radiofrequency ablation (RFA)±endoscopic resection (ER) is the preferred treatment for early neoplasia in Barrett's oesophagus (BE). We aimed to report short-term and long-term outcomes for all 1384 patients treated in the Netherlands (NL) from 2008 to 2018, with uniform treatment and follow-up (FU) in a centralised setting.

Endoscopic therapy for early BE neoplasia in NL is centralised in nine expert centres with specifically trained endoscopists and pathologists that adhere to a joint protocol. Prospectively collected data are registered in a uniform database. Patients with low/high-grade dysplasia or low-risk cancer, were treated by ER of visible lesions followed by trimonthly RFA sessions of any residual BE until complete eradication of BE (CE-BE). Patients with ER alone were not included.

After ER (62% of cases; 43% low-risk cancers) and median 1 circumferential and 2 focal RFA (p25-p75 0-1; 1-2) per patient, CE-BE was achieved in 94% (1270/1348). Adverse events occurred in 21% (268/1386), most commonly oesophageal stenosis (15%), all were managed endoscopically. A total of 1154 patients with CE-BE were analysed for long-term outcomes. During median 43 months (22-69) and 4 endoscopies (1-5), 38 patients developed dysplastic recurrence (3%, annual recurrence risk 1%), all were detected as endoscopically visible abnormalities. Random biopsies from a normal appearing cardia showed intestinal metaplasia (IM) in 14% and neoplasia in 0%. A finding of IM in the cardia was reproduced during further FU in only 33%, none progressed to neoplasia. Frequent FU visits in the first year of FU were not associated with recurrence risk.

In a setting of centralised care, RFA±ER is effective for eradication of Barrett's related neoplasia and has remarkably low rates of dysplastic recurrence. Our data support more lenient FU intervals, with emphasis on careful endoscopic inspection. Random biopsies from neosquamous epithelium and cardia are of questionable value.

NL7039.

Identification of Barrett's esophagus (BE) with the treatment of dysplasia is essential to prevent esophageal adenocarcinoma (EAC). Moreover, determination of BE prevalence is important to define subsequent management strategies. However, precise estimates on BE prevalence from several European countries are lacking. We aimed to determine BE prevalence in a Southern European country.

A cross-sectional, multicenter study from November 2019 to February 2020 was performed defining BE as a columnar extent in the distal esophagus greater than or equal to 1 cm with intestinal metaplasia.

A total of 1550 individuals, 51% male with a mean age of 62 (SD = 15) years undergoing upper endoscopy were included. The overall BE prevalence was 1.29% (95% confidence interval: 0.73-1.85); significantly higher in men [2.05% (1.06-3.04)] vs. women [0.53% (0.01-1.04)]. Of the 20 BE patients, eight were newly diagnosed and 12 were under surveillance. The median extent was C3 (min 0; max 16) M4.5 (min 2; max 16). One patient each had EAC (0.06%) and high-grade dysplasia (0.06%) at the time of endoscopy. There was no difference in prevalence between geographical regions, centers, use of sedation or experience of endoscopists. Considering all reports, 93% used standardized terminology, 23% accurate photodocumentation and 69% photodocumented the esophagogastric junction (EGJ). Furthermore, 80% used Prague classification, 55% Seattle protocol, 60% distance to the squamocolumnar junction, 75% to the EGJ and 40% to the hiatal pinch. When considering only reports with EGJ photodocumentation or Prague classification, the prevalence was 1.78% (0.91-2.64) or 1.03% (0.53-1.53).

We report for the first time BE prevalence in Southern Europe and report a low overall prevalence in an unselected population. Future studies need to determine progression rates and how to improve quality metrics.

Gastroesophageal reflux disease (GERD) is a chronic common disorder for which patients often refer to specialists. In the last decades, numerous studies helped to clarify the pathophysiology and the natural history of this disease. Currently, in the clinical setting, GERD is defined by the presence of symptoms that, when endoscopic investigation is required, permit to distinguish between cases with or without associated esophageal mucosal injuries. These conditions are called erosive reflux disease and non-erosive reflux disease (NERD), respectively. The latter is the most common manifestation of GERD. Symptoms are defined typical, as heartburn and regurgitation, and atypical (also called extra-esophageal), as coughing and/or wheezing, hoarseness, sore throat, otitis media, and dental manifestations. In this context, it is crucial for clinicians to investigate the presence of features of suspected malignancy, as unexplained weight loss, anemia, dysphagia, persistent vomiting, familiar history of cancer, long history of GERD, and beginning of GERD symptoms after the age of 50 years. The presence of these risk factors should induce to perform an endoscopic examination. Particular attention should be given to functional conditions that can mimic GERD, such as functional heartburn and hypersensitive esophagus as well as, more rarely, eosinophilic esophagitis. The former ones have different pathophysiology and this explains the frequent non-response to proton pump inhibitor drugs. This narrative review provides to clinicians a useful and practical overview of the state-of-the-art on advancements in the knowledge of GERD.

The causes for the occurrence of goblet cells at the gastroesophageal junction (GEJ-GC) are unknown. The aim of our study was to compare the concurrent histologic changes of the stomach in (1) patients with GEJ-GC, but without Barrett's esophagus (BE) to those in (2) patients with BE and in (3) controls without GEJ-GC or BE.

We used an electronic database of histopathologic records from 1.3 million individual patients, who underwent esophago-gastro-duodenoscopy (EGD) in 2009-2018. We compared the prevalence of Helicobacter pylori-positive gastritis (HpG), gastric intestinal metaplasia (G-IM), chronic inactive gastritis (CIG), and reactive gastropathy (RG) among the 3 patient groups, using odds ratios and their 95% confidence intervals.

Of all EGD patients, 4.0% harbored BE and 2.4% GEJ-GC. The average age of patients with GEJ-GC (60 ± 14) was significantly younger than the age of patients with BE (63 ± 12) and significantly older than the age of controls (55 ± 17). Female subjects were more common among GEJ-GC (54%) than BE (37%), but less common than among controls (63%). The 3 gastric histopathology changes associated with H. pylori were significantly more common in GEJ-GC than BE (for HpG 2.42, 2.29-2.56; for G-IM 1.82, 1.73-1.92; for CIG 1.31, 1.22-1.41). The corresponding differences between GEJ-GC and controls were less striking (for HpG 0.97, 0.93-1.01; for G-IM 1.15, 1.11-1.19; for CIG 0.90, 0.85-0.95). RG was slightly less common in GEJ-GC than BE (0.89, 0.86-0.92) and controls (0.94, 0.91-0.96).

With respect to its demographic and histopathologic features, GEJ-GC likely represents gastric intestinal metaplasia as opposed to BE and should prompt gastric intestinal metaplasia screening and management.

Determining the prevalence of Barrett's esophagus is important for defining screening strategies. We aimed to synthesize the available data, determine Barrett's esophagus prevalence, and assess variability.

Three databases were searched. Subgroup, sensitivity, and meta-regression analyses were conducted and pooled prevalence was computed.

Of 3510 studies, 103 were included. In the general population, we estimated a prevalence for endoscopic suspicion of Barrett's esophagus of (a) any length with histologic confirmation of intestinal metaplasia as 0.96% (95% confidence interval: 0.85-1.07), (b) ≥1 cm of length with histologic confirmation of intestinal metaplasia as 0.96% (95% confidence interval: 0.75-1.18) and (c) for any length with histologic confirmation of columnar metaplasia as 3.89% (95% confidence interval: 2.25-5.54) . By excluding studies with high-risk of bias, the prevalence decreased to: (a) 0.70% (95% confidence interval: 0.61-0.79) and (b) 0.82% (95% confidence interval: 0.63-1.01). In gastroesophageal reflux disease patients, we estimated the prevalence with afore-mentioned criteria to be: (a) 7.21% (95% confidence interval: 5.61-8.81) (b) 6.72% (95% confidence interval: 3.61-9.83) and (c) 7.80% (95% confidence interval: 4.26-11.34). The Barrett's esophagus prevalence was significantly influenced by time period, region, Barrett's esophagus definition, Seattle protocol, and study design. There was a significant gradient East-West and North-South. There were minimal to no data available for several countries. Moreover, there was significant heterogeneity between studies.

There is a need to reassess the true prevalence of Barrett's esophagus using the current guidelines in most regions. Having knowledge about the precise Barrett's esophagus prevalence, diverse attitudes from educational to screening programs could be taken.

There is controversy about finding intestinal metaplasia (IM) of the gastric cardia on biopsy. The most recent American College of Gastroenterology guideline comments that IM cardia is not more common in patients with Barrett's esophagus (BE). It provides limited guidance on whether the cardia should be treated when patients with BE undergo endoscopic eradication therapy (EET) and whether the cardia should undergo biopsy after ablation. The aims of our study were to determine the frequency in the proximal stomach of (1) histologic gastric cardia mucosa and (2) IM cardia. A third aim was to explore the frequency of advanced pathology (dysplasia and adenocarcinoma) in the cardia after patients with BE have undergone EET.

Consecutive patients undergoing esophagogastroduodenoscopy between January 2008 and December 2014 who had proximal stomach biopsies were included. Patients who had histologically confirmed BE were compared with those without BE.

Four hundred sixty-two patients, 289 with BE and 173 without BE, were included. Histologically confirmed cardiac mucosa was found in 81.6% of all patients. This was more frequent in those with versus without BE (86% vs 75%; odds ratio [OR], 2.06; 95% confidence interval [CI], 1.28-3.32; P = .003). IM cardia was more common in the BE group (17% vs 7%; OR, 2.67; 95% CI, 1.38-5.19; P = .004). Advanced pathology was more likely in the patients with BE who had undergone EET.

Cardiac mucosa is present in most patients who undergo endoscopy for upper GI symptoms. IM cardia is more common in patients with BE than those without. Advanced histologic changes in the cardia were seen only in the subgroup of patients with BE who had undergone EET.

Endoscopic eradication therapy is effective and durable for the treatment of Barrett's esophagus (BE), with low rates of recurrence of dysplasia but significant rates of recurrence of intestinal metaplasia. Identified risk factors for recurrence include age and length of BE before treatment and may also include presence of a large hiatal hernia, higher grade of dysplasia before treatment, and history of smoking. Current guidelines for surveillance following ablation are limited, with recommendations based on low-quality evidence and expert opinion. New modalities including optical coherence tomography and wide-area tissue sampling with computer-assisted analysis show promise as adjunctive surveillance modalities.

Barrett's esophagus (BE) is among the most common conditions encountered by the gastroenterologist. In this document, the American College of Gastroenterology updates its guidance for the best practices in caring for these patients. These guidelines continue to endorse screening of high-risk patients for BE; however, routine screening is limited to men with reflux symptoms and multiple other risk factors. Acknowledging recent data on the low risk of malignant progression in patients with nondysplastic BE, endoscopic surveillance intervals are attenuated in this population; patients with nondysplastic BE should undergo endoscopic surveillance no more frequently than every 3-5 years. Neither routine use of biomarker panels nor advanced endoscopic imaging techniques (beyond high-definition endoscopy) is recommended at this time. Endoscopic ablative therapy is recommended for patients with BE and high-grade dysplasia, as well as T1a esophageal adenocarcinoma. Based on recent level 1 evidence, endoscopic ablative therapy is also recommended for patients with BE and low-grade dysplasia, although endoscopic surveillance continues to be an acceptable alternative. Given the relatively common recurrence of BE after ablation, we suggest postablation endoscopic surveillance intervals. Although many of the recommendations provided are based on weak evidence or expert opinion, this document provides a pragmatic framework for the care of the patient with BE.

The prevalence of gallstones in patients with Barrett's esophagus (BE) and their gallbladder motility relative to that of healthy volunteers and GERD patients without BE were investigated. Of the 707 patients reviewed, 203 (125 males and 78 females) had BE. The prevalence of gallstones was significantly higher in the patients with BE than in those without BE (34 vs. 20%, respectively). The gallbladder functions of 22 patients with GERD, 27 patients with BE and 21 healthy volunteers were assessed by ultrasonography before and after a test meal. The patients with BE had significantly higher fasting volume and residual volume, but lower ejection volume, ejection fraction and ejection rate values than those of the healthy controls. None of the ultrasonographic parameters of patients without BE were significantly different from those of the controls. Patients with BE have a more complex gastrointestinal motility disorder that involves the gallbladder, and this makes this subset of patients with GERD more prone to gallstone disease.

Attention has focused on whether normalization, regression, and development of dysplasia and cancer in specialized intestinal metaplasia (SIM) differ among long-segment Barrett's esophagus (LSBE), short-segment BE (SSBE), and esophagogastric junction SIM (EGJSIM). We prospectively followed a cohort of SIM patients receiving long-term antisecretory medications to determine: (a) histologic normalization (no evidence of SIM on biopsy), (b) change in SIM length, (c) incidence of dysplasia and cancer, and (d) factors associated with normalization.

One hundred forty-eight patients with SIM were identified in our original cohort. Of these, 60.5% (23/38) LSBE, 69.8% (44/63) SSBE, and 72.3% (34/47) EGJSIM patients underwent repeat surveillance over a mean 44.4 +/- 9.7 months. Demographic, clinical, and endoscopic data were obtained.

(a) With long-term, antisecretory therapy, normalization occurred in 0/23 LSBE, 30% (13/44) of SSBE, and 68% (23/34) of EGJSIM (P < 0.001). (b) Normalization was more likely with EGJSIM (odds ratio [OR] 6.7, CI 2.3-19.3, P= 0.005), female gender (OR 7.3, CI 2.3-23.1, P= 0.001), or absence of hiatal hernia (OR 2.9, CI 1.02-8.06, P= 0.002). (c) A significant decrease in mean SIM length was noted for the entire population (2.5 +/- 0.3 to 2.13 +/- 0.3 cm, P= 0.004). (d) Follow-up incidence of dysplasia and cancer was 26.1% (3 indefinite, 2 low-grade dysplasia [LGD], 1 cancer) for LSBE, 6.8% (2 indefinite, 1 LGD) for SSBE, and none for EGJSIM (P < 0.004).

(a) Normalization of SIM occurs most frequently in EGJSIM>SSBE>LSBE. (b) Factors associated with normalization favor less severe GER and shorter segments of SIM. (c) Surveillance of LSBE results in the greatest yield for identifying dysplasia and cancer.

Intestinal metaplasia is a histologic hallmark of Barrett's esophagus and chronic gastritis. Intestinal metaplasia may progress to dysplasia or carcinomas without proper treatment. Most cases of intestinal metaplasia are easily recognized on hematoxylin and eosin-stained sections. However, some cases of intestinal metaplasia may be hard to recognize if they lack the characteristic mucin-producing cells and Paneth cells, or if they are small in size. Recently, keratin 7, keratin 20, and MUC2 expression patterns were reported to be useful in confirming the diagnosis of intestinal metaplasia. We studied hepatocyte (Hep) antigen (a hepatocellular antigen mainly expressing in normal and neoplastic hepatic tissues) in 33 cases of Barrett's esophagus (9 cases associated with esophageal adenocarcinoma) and 13 cases of chronic gastritis associated with intestinal metaplasia and gastric adenocarcinoma. Hep monoclonal antibody recognizes intestinal metaplasia in all cases. We also compared expression of Hep with that of keratin 7, keratin 20, and MUC2 in intestinal metaplasia. The specificity and sensitivity of Hep for intestinal metaplasia were higher than that of keratin 7 and keratin 20, or MUC2. We conclude that Hep may be used as a single diagnostic marker for intestinal metaplasia.

Previous studies present conflicting results regarding relationship between gastric emptying and gastro-oesophageal reflux disease. Reflux of duodenal content to oesophagus is generally considered to be associated with more severe disease.

To assess presence of a gastric emptying disorder in persons with reflux of duodenal contents to oesophagus and to identify any correlation with gastric emptying and oesophageal motility.

A total of 15 subjects with (B+) and 15 subjects without (B-) bile reflux to oesophagus determined by 24-hour bilirubin monitoring were studied with scintigraphic solid gastric emptying and 24-hour oesophageal manometry.

There was no difference in lag phase [median 23.7 (range 10.8-44.0) vs 24.6 (8.1-40.1) min], half emptying time [74.6 (48.0-93.6) vs 82.8 (54.4-153.9) min] or emptying rate [0.89 (0.59-1.34) vs 0.83 (0.36-1. 15)%/min] for B- and B+ subjects, respectively. In addition, there was no difference in emptying rate of gastric fundus between B- and B+ subjects. Subjects with bile reflux had less effective oesophageal contractions of oesophageal body [9.4(3.3-37)%] compared to subjects without bile reflux [32(19-47)%, p = 0.002]. However, there was no correlation between oesophageal motility and gastric emptying.

Results suggest that a gastric emptying disorder is a less likely contributing cause of bile reflux to the oesophagus, but bile reflux is associated with less effective oesophageal motility.

Barrett's oesophagus is defined as specialised intestinal metaplasia in the distal oesophagus, regardless of extension.

To study distal oesophagus function, and acid and bile exposure in patients with Long Segment (>3 cm), Short Segment (1 to 2 cm) and Ultra-short Segment (<1 cm) Barrett's Oesophagus, and in patients with gastro-oesophageal reflux disease without intestinal metaplasia.

Study population comprised 17 patients with Long, 8 with Short, 9 with Ultra-Short Segment Barrett's oesophagus, 32 with reflux disease and 12 healthy volunteers.

Patients were evaluated by manometry and by 24-hour pH and bile monitoring.

Patients with intestinal metaplasia had greater acid exposure of the distal oesophagus than healthy volunteers. Patients with Long Segment Barrett's oesophagus had a longer history of symptoms, worse lower oesophageal sphincter pressures and longer bile and acid exposure than the other patients. Long Segment Barrett's oesophagus was predicted by low oesophageal pressure and increased bile exposure, age and male sex.

Acid exposure in the distal oesophagus is probably the aetiological factor behind intestinal metaplasia, but a severely damaged antireflux barrier and bile in the refluxate are necessary for Long Segment Barrett's Oesophagus to develop.