This patient presents Barrett's esophagus with low grade dysplasia. I do not like the question, since not being with acid production inhibition the dysplasia may be conditioned by inflammation and not be real. In any case, Barrett's esophagus should follow endoscopic surveillance and lifelong PPI treatment or antireflux surgery to prevent progression. The correct answer is 4.

This patient presents Barrett's esophagus with low grade dysplasia. I do not like the question, since not being with acid production inhibition the dysplasia may be conditioned by inflammation and not be real. In any case, Barrett's esophagus should follow endoscopic surveillance and lifelong PPI treatment or antireflux surgery to prevent progression. [HIDDEN]

A 66-year-old man reports daily heartburn since youth, which he treats with alkalis. An upper endoscopy shows mild erosive esophagitis and displaced squamous columnar junction approximately 7 cm. The esophageal biopsies showed mild erosive esophagitis and a columnar squamous junction displaced approximately 7 cm from the most proximal portion of the gastric folds. Biopsies of the distal esophagus reveal that the normal squamous epithelium has been replaced by intestinal-type columnar epithelium with low-grade dysplasia What is the most appropriate management option for this patient?

Given that the esophagitis is mild and the dysplasia is low grade, it is advisable to continue treatment with alkalines.

Indefinite treatment with high doses of PPI since it has been demonstrated that this prevents the progression of Barrett's esophagus to adenocarcinoma, making endoscopic surveillance unnecessary.

Periodic surveillance endoscopies and treatment with PPIs for less than 12 weeks, since prolonged treatment is associated with a high risk of gastrinoma development.

Periodic surveillance endoscopies and indefinite treatment with PPI.

Endoscopic surveillance in Barrett's esophagus.

Barrett's esophagus (BE), a complication of chronic gastroesophageal reflux disease (GORD), is a condition that is premalignant for adenocarcinoma of the esophagus and esophagogastric junction. Esophageal adenocarcinoma, once an uncommon entity, has been growing rapidly in incidence over the last two decades in several parts of the world. Barrett's esophagus is a change in the esophageal epithelium of any length that can be recognized at endoscopy and is confirmed to have intestinal metaplasia by biopsy (American College of Gastroenterology guidelines). Because of its premalignant nature, it is recommended that patients with BE undergo regular endoscopic surveillance. The recommendation for endoscopic surveillance is based on unproved and controversial assumptions including: 1) the assumption that Barrett's esophagus adversely influences survival; 2) the assumption that endoscopic surveillance can reliably detect early, curable neoplasia in the columnar lined esophagus. Moreover, the low incidence of adenocarcinoma (reported cancer incidence rates in prospective studies on BE range between 0.5% and 1.9%) is used to support an approach of not surveying patients with Barrett's esophagus. Despite these not convincing data, endoscopic surveillance is considered ''reasonable'' and ''desirable'' by the gastroenterological associations and consensus meetings. Endoscopic surveillance for cancer in Barrett's esophagus (BE) is performed primarily to seek dysplasia, to prevent the progression to invasive malignancy; however, one of the limitations of using dysplasia is a lack of understanding of its natural history. The efficacy of endoscopic surveillance for Barrett's esophagus is likely to remain unclear for a long time. The American College of Gastroenterology has recommended the following practice guidelines: a) for patients with no dysplasia, surveillance endoscopy is recommended at an interval of every 2 to 3 years; b) for patients with low grade dysplasia, surveillance endoscopy every 6 months for the first year is recommended, followed by yearly endoscopy if the dysplasia has not progressed in severity; c) for patients with high grade dysplasia, two alternatives are proposed after the diagnosis has been confirmed by an expert gastrointestinal pathologist. One alternative is intensive endoscopic surveillance until intramucosal cancer is detected at an interval of every 3-6 months. The other alternative is esophageal resection. In the situation of indeterminate dysplasia, whereas the pathologist can not come to definite diagnosis, control biopsies are proposed after 2 months of adequate acid suppression by means of proton pump inhibition. In all cases, the technique of random, four quadrant biopsies taken every 2 cm in the columnar-lined esophagus for standard histologic evaluation is recommended. Any grossly abnormal areas may be biopsied too. One can expect however that during the next future these protocol will change considering new data on dysplasia detection (biochemical markers, flow cytometry), new techniques to identify dysplasia (chromoendoscopy, endosonography, coherence optical tomography, fluorescence techniques) and development of better ablative techniques. At present a marker other than dysplasia identifying a high risk group for cancer on which to focus endoscopic surveillance has not yet been established.

Diagnosis and Management of Low-Grade Dysplasia in Barrett's Esophagus: Expert Review From the Clinical Practice Updates Committee of the American Gastroenterological Association.

The purpose of this clinical practice update expert review is to define the key principles in the diagnosis and management of low-grade dysplasia (LGD) in Barrett's esophagus patients. The best practices outlined in this review are based on relevant publications, including systematic reviews and expert opinion (when applicable). Practice Advice 1: The extent of Barrett's esophagus should be defined using a standardized grading system documenting the circumferential and maximal extent of the columnar lined esophagus (Prague classification) with a clear description of landmarks and visible lesions (nodularity, ulceration) when present. Practice Advice 2: Given the significant interobserver variability among pathologists, the diagnosis of Barrett's esophagus with LGD should be confirmed by an expert gastrointestinal pathologist (defined as a pathologist with a special interest in Barrett's esophagus-related neoplasia who is recognized as an expert in this field by his/her peers). Practice Advice 3: Expert pathologists should report audits of their diagnosed cases of LGD, such as the frequency of LGD diagnosed among surveillance patients and/or the difference in incidence of neoplastic progression among patients diagnosed with LGD vs nondysplastic Barrett's esophagus. Practice Advice 4: Patients in whom the diagnosis of LGD is downgraded to nondysplastic Barrett's esophagus should be managed as nondysplastic Barrett's esophagus. Practice Advice 5: In Barrett's esophagus patients with confirmed LGD (based on expert gastrointestinal pathology review), repeat upper endoscopy using high-definition/high-resolution white-light endoscopy should be performed under maximal acid suppression (twice daily dosing of proton pump inhibitor therapy) in 8-12 weeks. Practice Advice 6: Under ideal circumstances, surveillance biopsies should not be performed in the presence of active inflammation (erosive esophagitis, Los Angeles grade C and D). Pathologists should be informed if biopsies are obtained in the setting of erosive esophagitis and if pathology findings suggest LGD, or if no biopsies are obtained, surveillance biopsies should be repeated after the anti-reflux regimen has been further intensified. Practice Advice 7: Surveillance biopsies should be performed in a four-quadrant fashion every 1-2 cm with target biopsies obtained from visible lesions taken first. Practice Advice 8: Patients with a confirmed histologic diagnosis of LGD should be referred to an endoscopist with expertise in managing Barrett's esophagus-related neoplasia practicing at centers equipped with high-definition endoscopy and capable of performing endoscopic resection and ablation. Practice Advice 9: Endoscopic resection should be performed in Barrett's esophagus patients with LGD with endoscopically visible abnormalities (no matter how subtle) in order to accurately assess the grade of dysplasia. Practice Advice 10: In patients with confirmed Barrett's esophagus with LGD by expert GI pathology review that persists on a second endoscopy, despite intensification of acid-suppressive therapy, risks and benefits of management options of endoscopic eradication therapy (specifically adverse events associated with endoscopic resection and ablation), and ongoing surveillance should be discussed and documented. Practice Advice 11: Endoscopic eradication therapy should be considered in patients with confirmed and persistent LGD with the goal of achieving complete eradication of intestinal metaplasia. Practice Advice 12: Patients with LGD undergoing surveillance rather than endoscopic eradication therapy should undergo surveillance every 6 months times 2, then annually unless there is reversion to nondysplastic Barrett's esophagus. Biopsies should be obtained in 4-quadrants every 1-2 cm and of any visible lesions. Practice Advice 13: In patients with Barrett's esophagus-related LGD undergoing ablative therapy, radiofrequency ablation should be used. Practice Advice 14: Patients completing endoscopic eradication therapy should be enrolled in an endoscopic surveillance program. Patients who have achieved complete eradication of intestinal metaplasia should undergo surveillance every year for 2 years and then every 3 years thereafter to detect recurrent intestinal metaplasia and dysplasia. Patients who have not achieved complete eradication of intestinal metaplasia should undergo surveillance every 6 months for 1 year after the last endoscopy, then annually for 2 years, then every 3 years thereafter. Practice Advice 15: Following endoscopic eradication therapy, the biopsy protocol of obtaining biopsies in 4 quadrants every 2 cm throughout the length of the original Barrett's esophagus segment and any visible columnar mucosa is suggested. Practice Advice 16: Endoscopists performing endoscopic eradication therapy should report audits of their rates of complete eradication of dysplasia and intestinal metaplasia and adverse events in clinical practice.

Barrett's esophagus: A historical perspective, an update on core practicalities and predictions on future evolutions of management.

Interpretation of exploding knowledge about Barrett's esophagus is impaired by use of several conflicting definitions. Because any histological type of esophageal columnar metaplasia carries risk for esophageal adenocarcinoma, the diagnosis of Barrett's esophagus should no longer require demonstration of intestinal-type metaplasia. Endoscopic recognition and grading of Barrett's esophagus remains a significant source of ambiguity. Reflux disease is a key factor for development of Barrett's esophagus, but other factors must underlie its development, since it occurs in only a minority of reflux disease patients. Neither antireflux surgery nor proton pump inhibitor (PPI) therapy has major impacts on cancer risk. Within a year, a major trial should indicate whether low-dose aspirin usefully reduces cancer risk. The best referral centers have transformed the accuracy of screening and surveillance for early curable esophageal adenocarcinoma by use of enhanced and novel endoscopic imaging, visually-guided, rather than blind biopsies and by partnership with expert pathologists. General endoscopists now need to upgrade their skills and equipment so that they can rely mainly on visual targeting of biopsies on mucosal areas of concern in their surveillance practice. General pathologists need to greatly improve their interpretation of biopsies. Endoscopic therapy now achieves very high rates of cure of high-grade dysplasia and esophageal adenocarcinoma with minimal morbidity and risk. Such results will only be achieved by skilled interventional endoscopists. Esophagectomy should now be mainly restricted to patients whose cancer has extended into and beyond the submucosa. Weighing risks and benefits in the management of Barrett's esophagus is difficult, as is the process of adequately informing patients about their specific cancer risk.

How should we describe, diagnose and observe the Barrett's esophagus?

Barrett's esophagus (BE) is one of the major complications of gastroesophageal reflux disease (GERD) commonly encountered in gastroenterology clinics. A consensus has not been achieved yet with respect to the definition of BE in published guidelines. It is advised to use the Prague classification and not to use the definition of short and long segments for the endoscopic standardization of BE. Undertaking biopsies with white-light endoscopy from each of the 4 quadrants at 2-cm intervals is the standard method for the diagnosis of BE. Because of the ability to perform targeted biopsies, the available data indicate that advanced endoscopic techniques may reduce the number of biopsies needed for diagnoses. In the presence of severe esophagitis along with BE, the biopsies should be taken after 8 weeks of PPI therapy. The evidence values of the suggestions about the surveillance requirements and surveillance frequencies are low because the available data mostly rely on retrospective studies. We suggest that all the patients with BE should be referred to specialized centers for surveillance in Turkey. Considering the additional risk factors of the patient, endoscopy surveillance intervals of the patients with BE without dysplasia should be in a range of 3-5 years and annual surveillance should be made in BE with low-grade dysplasia. In the presence of BE with high-grade dysplasia (HGD), the patients should be referred to specialized centers for treatment within 3 months at the latest.

Barrett's esophagus. Diagnosis, follow-up and treatment.

Barrett's Esophagus (BE) is a premalignant condition in the esophagus. Esophageal adenocarcinomas have the fastest increase of incidence of all solid tumors in the western world. BE is defined as areas with macroscopic visible columnar epithelium and intestinal metaplasia oral of the anatomical gastroesophageal junction. The extent of the endoscopic findings is described by the Prague classification. The metaplasia is histologically confirmed by the presence of intestinal metaplasia. The diagnosis of BE can only be made by a combined macroscopic and microscopic examination. The histological description should include evaluation of dysplasia, and if present it should be classified as low or high grade dysplasia. All patients are offered relevant antireflux treatment with PPI or surgery. Ablation or mucosal resection of metaplastic epithelia with or without low grade dysplasia is experimental and it is not recommended outside controlled studies. Treatment of high grade dysplasia and carcinoma in situ is handled in departments treating esophageal cancer. Follow-up with endoscopy and biopsy can be offered. Follow-up endoscopy with biopsy can only be recommended after thorough information to the patients, as evidence for the value is scarce.

Barrett's esophagus

Diagnosis Both macroscopic (from endoscopy) and microscopic positive findings are required to make a diagnosis. Barrett's esophagus is marked by the presence of columnar epithelia in the lower esophagus, replacing the normal squamous cell epithelium—an example of metaplasia. The secretory columnar epithelium may be more able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased risk of adenocarcinoma. Screening Screening endoscopy is recommended among males over the age of 60 who have reflux symptoms that are of long duration and not controllable with treatment. Among those not expected to live more than 5 years screening is not recommended. The Seattle protocol is used commonly in endoscopy to obtain endoscopic biopsies for screening, taken every 1 to 2 cm from the gastroesophageal junction.

Recent developments in gastroesophageal reflux disease and Barrett's esophagus: ANNO 2012.

The incidence of gastroesophageal reflux disease (GERD) and esophageal columnar metaplasia is rising worldwide. Both mechanical and functional factors perturb the double sphincter barrier at the esophagogastric junction (EGJ). Discovery of the acid pocket is fundamental in understanding postprandial acid reflux. Adding impedencemetry to pH measurements allows detection of non-acid or weakly acidic reflux. Histologic and endoscopic injury of the squamous mucosa rises from dilation of the intercellular spaces, papillary extension, accentuated intrapapillary looping, red streaks, erosive tissue loss, etc., graded with the Los Angeles system. Seventy percent of patients have no recognizable abnormalities (non-erosive or neGERD). Treatment of GERD mainly relates to the control of acid secretion but a revival of alginate/antacid obliterating the acid pocket is to be expected. Weaker heartburn control in neGERD is a misnomer because most studies included patients with no evidence of reflux disease. Traditional (delayed-release) proton pump inhibitors (PPIs) are powerful suppressors of acid secretion but do have limitations such as gradual build up of acid control, weak control of nocturnal acid recovery, possibility of rebound, occasional need for dose escalation, etc. Barrett's esophagus (BE) is endoscopically diagnosed also in the absence of intestinal metaplasia. A prerequisite is the precise location of the EGJ (proximal end of gastric folds, esophageal sphincter pinch, distal extent of palisade vessels). BE is graded with the Prague C & M system. Barrett's cancer develops usually via low-grade and high-grade dysplasia. Endoscopic examination may indicate suspicious areas, amenable for targeted biopsy. Otherwise, four quadrant biopsies are obtained when searching for neoplasia. Low-grade dysplasia, especially when it is multifocal and p53 positive, high-grade dysplasia and mucosal cancer should be treated with endoscopic resection of the target area, followed by radiofrequency ablation of the adjacent non-neoplastic columnar mucosa, followed with powerful acid suppressant therapy. The long-term results of the combination of resection and ablation are exiting and at least comparable to surgical resection.

Barrett's esophagus

The main cause of Barrett's esophagus is thought to be an adaptation to chronic acid exposure from reflux esophagitis. Barrett's esophagus is diagnosed by endoscopy: observing the characteristic appearance of this condition by direct inspection of the lower esophagus; followed by microscopic examination of tissue from the affected area obtained from biopsy. The cells of Barrett's esophagus are classified into four categories: nondysplastic, low-grade dysplasia, high-grade dysplasia, and frank carcinoma. High-grade dysplasia and early stages of adenocarcinoma may be treated by endoscopic resection or radiofrequency ablation. Later stages of adenocarcinoma may be treated with surgical resection or palliation. Those with nondysplastic or low-grade dysplasia are managed by annual observation with endoscopy, or treatment with radiofrequency ablation. In high-grade dysplasia, the risk of developing cancer might be at 10% per patient-year or greater.

Detection of Barrett's esophagus after endoscopic healing of erosive esophagitis.

The presence of erosive esophagitis (EE) in patients presenting for upper endoscopy may prevent the detection of underlying Barrett's esophagus (BE) in the distal esophagus. To prospectively determine the proportion of patients detected with BE upon repeat endoscopy after healing of EE. Patients with endoscopically confirmed EE without BE were treated with standard doses of acid suppression therapy and a repeat endoscopy was performed to assess the presence of BE. If columnar mucosa was visualized in the distal esophagus, targeted biopsies were obtained and all biopsies were evaluated for the presence of intestinal metaplasia. BE was defined as columnar mucosa in the distal esophagus with intestinal metaplasia on biopsy. A total of 172 patients with reflux symptoms were diagnosed with EE without BE on initial endoscopy. They were treated with standard doses of proton pump inhibitor therapy, and after a mean duration of 11 wk (range 8-16 wk), a repeat endoscopy was performed to confirm healing of EE and to document the presence of BE. On repeat endoscopy, EE was completely healed in 116 patients (67%), and of those, BE was suspected in 32 patients (i.e., columnar-lined distal esophagus) and was confirmed in 16 patients (13.8%). In the 56 patients with persistent EE on repeat endoscopy, columnar mucosa in areas of previously healed esophagitis was visualized in 8 and confirmed in 5 patients (8.9% of nonhealed cases). Overall, 21 (12%) patients were confirmed with BE on repeat endoscopy; all men, mean age 61 yr with a median BE length of 0.5 cm (range 0.5-5 cm, interquartile range 0.5 cm). The majority of these patients (N = 19) had short segment Barrett's esophagus (SSBE) (i.e., length <3 cm). In patients with EE undergoing treatment with acid suppressive therapy, BE (mainly SSBE) is detected in approximately 12% of patients on repeat endoscopy. Patients with reflux symptoms undergoing endoscopy for the detection of BE (i.e., screening) should be treated with acid suppressive therapy prior to endoscopy to enhance the yield of BE. Alternatively, if the goal is to document BE and if EE is found at the initial endoscopy, then repeat endoscopy may be considered after acid suppressive therapy.

Reflux Esophagitis  -- Evaluation

Patients with atypical symptoms should undergo a diagnostic evaluation with endoscopy and pH monitoring before a PPI trial. Barium studies to diagnose reflux esophagitis are of limited value. The presence or absence of reflux during barium esophagography does not correlate with the incidence or extent of reflux observed during 24-hour pH impedance monitoring and is of no value in the diagnosis of reflux esophagitis. [55] Los Angeles classification of severity of reflux esophagitis-four grades: [56] Grade A: One or more esophageal mucosal breaks less than 5 mm in length. Grade B: One or more mucosal breaks greater than 5 mm but with continuity across mucosal folds. Grade C: Continuous mucosal breaks between the tops of two or more mucosal folds but involving less than 75% of the esophageal circumference. Grade D: Mucosal breaks involving more than 75% of the esophageal sphincter.

Squamous islands in Barrett's esophagus: what lies underneath?

Squamous islands are frequently visualized at the time of upper endoscopy in patients with Barrett's esophagus, especially those on proton pump inhibitor therapy (PPI). The significance of these islands is not clearly understood. The aim of this study was to systematically biopsy macroscopic squamous islands and to examine their histologic characteristics. Patients with Barrett's esophagus undergoing surveillance had squamous islands documented and biopsied at the time of endoscopy. Barrett's esophagus was defined as the presence of a columnar lined esophagus on endoscopy with intestinal metaplasia on biopsy. All biopsies were obtained by a single senior endoscopist and were stained with alcian blue at pH 2.5. Biopsy samples with inadequate tissue quantity were not included in the study. A total of 39 biopsies were obtained from 22 patients. Twenty of the 22 patients were male, with a mean age of 65.4 yr (range 47-80 yr). The mean length of Barrett's mucosa was 5.6 cm (range 1-11 cm). Eleven of 22 patients were on omeprazole (mean dose 29.1 mg/day), whereas seven patients were on lansoprazole (60 mg/day). The mean duration of PPI therapy was 2.3 yr (range 9-71 months) at the time of biopsy of the squamous islands. Three patients were on H2-blocker therapy whereas the remaining patient had not been started on acid suppression therapy. On histology, 24 biopsy specimens (61.5%) revealed only squamous epithelium, whereas 15 (38.5%) showed the presence of intestinal metaplasia underlying the squamous epithelium. There was no significant difference between the patients with and without underlying intestinal metaplasia in regard to age, Barrett's length, dose, and duration of PPI therapy. In more than one-third of biopsies of macroscopic squamous islands within Barrett's esophagus, microscopic intestinal metaplasia is detected. The presence of squamous islands should not be equated with regression of Barrett's esophagus or with decreased cancer risk.

Eosinophilic esophagitis

Esophageal mucosal biopsy Currently, endoscopic mucosal biopsy remains the most important diagnostic test for EoE, and is required to confirm the diagnosis. Biopsy specimens from both the proximal/mid and distal esophagus should be obtained regardless of the gross appearance of the mucosa. Specimens should also be obtained from areas revealing endoscopic abnormalities. At least four biopsies are required to obtain adequate sensitivity for the detection of EoE. A definitive diagnosis of EoE is based on the presence of at least 15 eosinophils/HPF in the esophageal biopsies of patients despite treatment with high-dose PPI. GERD can increase eosinophilic infiltration in the distal esophagus, however, eosinophils associated with GERD generally occur at a lower density (i.e. < 15/HPF).

Barrett Esophagus -- Treatment / Management

Surveillance plan strategies have a history of being arbitrary and not validated by strong prospective clinical studies with a 2014 study, even concluding that there is no association between surveillance and decreased EAC-related deaths. Based on their systematic review of the literature and evaluation of the level of evidence, the ACG made several changes to the recommended management of BE in its newest guidelines. High-definition white-light endoscopy is a novel endoscopic technology that is now recommended for routine use in surveillance beyond electronic chromoendoscopy. For non-dysplastic BE, the current ACG recommendation after the initial diagnosis is to follow up with surveillance every 3 to 5 years. The patient should also be placed on once-daily proton pump inhibitor therapy, regardless of the presence of reflux symptoms, due to evidence of a chemopreventive effect of proton pump inhibitors, where the risk of progression to neoplastic BE is reduced compared to no acid suppression or H2 blockers. Due to the significant impact on management, if BE is associated with dysplasia, the ACG emphasizes the importance of confirming a dysplasia diagnosis with a second pathologist with extensive experience in BE-related neoplasia. Patients with confirmed low-grade dysplasia can now be considered for endoscopic ablative therapy or can follow a 6 to 12-month interval surveillance plan.  For patients with confirmed high-grade dysplasia with endoscopic mucosal abnormalities, endoscopic mucosal resection followed by ablation of the remaining BE mucosa is recommended.  If no mucosal abnormality is visible, in other words, the mucosa is flat; radiofrequency ablation therapy is considered sufficient for low- or high-grade dysplasia as well as carcinoma. Cryotherapy is another option of ablative therapy.  It is necessary to continue surveillance of patients after ablative therapy, as multiple treatments are often required to ensure complete elimination of the lesional tissue. Surgical therapies such as esophagectomy are not the preferred initial approach to management for high-grade dysplasia or intramucosal cancer, as the procedure has a high risk of morbidities, though should be considered if intramucosal cancer has poor prognostic factors, such as lymphovascular invasion or poor differentiation or if cancer involves the submucosa. Patients with significant comorbidities that limit their likely survival may not benefit from endoscopic therapies, with risks of the procedures being greater than potential gains. [14] [15]

Surgery_Schwartz

7% of patients following antireflux surgery. About 15% of patients had abnormal acid exposure after surgery. Although pH data were not routinely collected in patients on PPI therapy, in the subgroup of 12 patients that did have 24-hour monitoring on treat-ment, 3 of 12 (25%) had persistently high esophageal acid expo-sure, and most (75%) had persistently high bilirubin exposure.The common belief that Barrett’s epithelium cannot be reversed by antireflux surgery may not be correct. Within the control arm of a randomized trial of ablation vs. surveillance, Bright and associates identified approximately 50% regression in the length of Barrett’s esophagus in 20 patients within the control arm of a randomized trial of ablation vs. surveillance.Current data indicate that patients with BE should remain in an endoscopic surveillance program following antireflux surgery. Biopsy specimens should be reviewed by a patholo-gist with expertise in the field. If low-grade dysplasia is con-firmed,

Barrett esophagus.

The importance of an in-depth understanding about Barrett esophagus is ultimately to decrease the mortality and morbidity from esophageal adenocarcinoma cancer by early detection of metaplasia and dysplasia and appropriate therapy. This review summarizes several publications in the past year related to the epidemiology, pathogenesis, screening and surveillance, new methods for detection of metaplasia/dysplasia, and advances in the treatment of Barrett esophagus. Patients with Barrett esophagus are characterized by the presence of risk factors usually indicative of severe types of gastroesophageal reflux disease. Recent insights into epidemiology and pathogenesis have shown that the risk of high-grade dysplasia and adenocarcinoma may be related to the increasing length of Barrett esophagus, size of hiatus hernia, and severity of acid reflux. The role of smoking and alcohol consumption remains controversial. Increasing the number of biopsies by repeat standard endoscopy can enhance the yield of intestinal metaplasia in patients with suspected short-segment Barrett esophagus. Costs of surveillance using standard endoscopy and random biopsies would be very high and using special techniques to target specific areas could ultimately help in cost reduction. Emerging data on new techniques and technology such as vital staining with methylene blue and protoporphyrin fluorescence can increase the yield of metaplasia and dysplasia. Biomarkers studies have revealed that p53 mutation by the loss of heterozygosity can help detect patients with low and high risk for cancer progression. Studies thus far have been unclear whether acid suppression alone can impact the malignant progression in Barrett esophagus patients. Inhibition of cyclooxygenase by aspirin or nonsteroidal anti-inflammatory drugs may be a promising chemoprevention strategy against dysplasia and esophageal adenocarcinoma development as shown in some recent studies. Nonsurgical treatment by photodynamic therapy or mucosal resection may be a less invasive and organ-sparing option for some patients with high-grade dysplasia and early adenocarcinoma. In the past year we have made major strides in our knowledge of this premalignant lesion. Recent studies have shed light in a better understanding of the epidemiology of Barrett esophagus, including clinical and endoscopic factors associated with high-grade dysplasia or esophageal adenocarcinoma and various biomarkers that would identify patient subsets with low and high risk for cancer progression. This will eventually have significant implications on the screening, surveillance, and treatment of the disease. Advanced endoscopic therapies including mucosectomy or photodynamic therapy may be emerging options in patients with intraepithelial neoplasia.

Reflux Esophagitis  -- Treatment / Management

Maintain PPI therapy for patients who continue to have symptoms and patients with erosive esophagitis and Barrett esophagus.

Results of short-and long-term medical treatment of gastroesophageal reflux disease (GERD).

Symptomatic esophageal reflux affects a large number of individuals. Many find relief by avoiding trigger substances such as coffee or sweets; in other cases, lifestyle modifications do not suffice and drug treatment is necessary for symptom control. An adequate classification of gastroesophageal reflux disease (GERD) is currently lacking; esophagitis can be graded according to Savary and Miller or the more recent metaplasia ulcer stricture erosions (MUSE) classification. The control of symptoms should be achieved in all patients: in addition, if esophagitis is present, the healing of erosions/ulcers as well as the prevention of further complications, such as strictures, hemorrhage, Barrett's esophagus or ulceration, must be accomplished. SHORT-TERM TREATMENT: In the case of rare symptoms, control might be achieved by lifestyle modifications and by antacids or mucosal protectants taken on demand. In the case of continuous symptoms or signs of esophagitis, effective inhibition of gastric acid secretion with proton pump inhibitors (PPIs) is necessary in many patients. After discontinuation of medical therapy, almost all patients with esophagitis will experience a relapse within 30 weeks. The regimen offering the highest rate of remission in these patients is the one that induced remission in the first place. Reduction of PPI dose or a switch to H2 receptor antagonists increases the rate of relapse. RISKS OF LONG-TERM TREATMENT: Long-term acid suppressive therapy, as with the use of PPIs, may lead to hypergastrinemia, a situation in which the endocrine cells of the stomach may proliferate. In the presence of Helicobacter pylori infection, PPIs are more efficient in healing esophagitis; however, the occurrence of gastric mucosal atrophy, a potentially pre-cancerous condition, has been described. To date, however, no case of gastric cancer or endocrine neoplasia associated with PPI treatment has been documented; gastric mucosal atrophy is more likely to result from H. pylori infection and gastric carcinoid formation needs a genetic predisposition, such as multiple endocrine neoplasia (MEN) type I. Most cases of GERD can be effectively treated by non-surgical measures; in patients presenting with warning symptoms or persistent heartburn, endoscopy of the upper gastrointestinal tract is mandatory. Long-term use of PPIs seems to be a safe and efficient treatment for GERD. For the prevention of relapse, similar doses are needed as for the induction of remission in reflux esophagitis.

AGA Clinical Practice Update on Endoscopic Treatment of Barrett's Esophagus With Dysplasia and/or Early Cancer: Expert Review.

The purpose of this best practice advice article is to describe the role of Barrett's endoscopic therapy (BET) in patients with Barrett's esophagus (BE) with dysplasia and/or early cancer and appropriate follow-up of these patients. The best practice advice provided in this document is based on evidence and relevant publications reviewed by the committee. BEST PRACTICE ADVICE 1: In BE patients with confirmed low-grade dysplasia, a repeat examination with high-definition white-light endoscopy should be performed within 3-6 months to rule out the presence of a visible lesion, which should prompt endoscopic resection. BEST PRACTICE ADVICE 2: Both BET and continued surveillance are reasonable options for the management of BE patients with confirmed and persistent low-grade dysplasia. BEST PRACTICE ADVICE 3: BET is the preferred treatment for BE patients with high-grade dysplasia (HGD). BEST PRACTICE ADVICE 4: BET should be preferred over esophagectomy for BE patients with intramucosal esophageal adenocarcinoma (T1a). BEST PRACTICE ADVICE 5: BET is a reasonable alternative to esophagectomy in patients with submucosal esophageal adenocarcinoma (T1b) with low-risk features (<500-μm invasion in the submucosa [sm1], good to moderate differentiation, and no lymphatic invasion) especially in those who are poor surgical candidates. BEST PRACTICE ADVICE 6: In all patients undergoing BET, mucosal ablation should be applied to 1) all visible esophageal columnar mucosa; 2) 5-10 mm proximal to the squamocolumnar junction and 3) 5-10 mm distal to the gastroesophageal junction, as demarcated by the top of the gastric folds (ie, gastric cardia) using focal ablation in a circumferential fashion. BEST PRACTICE ADVICE 7: Mucosal ablation therapy should only be performed in the presence of flat BE without signs of inflammation and in the absence of visible abnormalities. BEST PRACTICE ADVICE 8: BET should be performed by experts in high-volume centers that perform a minimum of 10 new cases annually. BEST PRACTICE ADVICE 9: BET should be continued until there is an absence of columnar epithelium in the tubular esophagus on high-definition white-light endoscopy and preferably optical chromoendoscopy. In case of complete endoscopic eradication, the neosquamous mucosa and the gastric cardia are sampled by 4-quadrant biopsies. BEST PRACTICE ADVICE 10: If random biopsies obtained from the neosquamous epithelium demonstrate intestinal metaplasia/dysplasia or subsquamous intestinal metaplasia, a repeat endoscopy should be performed and visible islands or tongues should undergo targeted focal ablation. BEST PRACTICE ADVICE 11: Intestinal metaplasia of the gastric cardia (without residual columnar epithelium in the tubular esophagus) should not warrant additional ablation therapy. BEST PRACTICE ADVICE 12: When consenting patients for BET, the most common complication of therapy to be quoted is post-procedural stricture formation, occurring in about 6% of cases. Bleeding and perforation occur at rates <1%. BEST PRACTICE ADVICE 13: After complete eradication (endoscopic and histologic) of intestinal metaplasia has been achieved with BET, surveillance endoscopy with biopsies should be performed at the following intervals: for baseline diagnosis of HGD/esophageal adenocarcinoma: at 3, 6, and 12 months and annually thereafter; and baseline diagnosis of low-grade dysplasia: at 1 and 3 years. BEST PRACTICE ADVICE 14: Endoscopic surveillance post therapy should be performed with high-definition white-light endoscopy, including careful inspection of the neosquamous mucosal and retroflexed inspection of the gastric cardia. BEST PRACTICE ADVICE 15: The approach to recurrent disease is similar to that of the initial therapy; visible recurrent nodular lesions require endoscopic resection, whereas flat areas of columnar mucosa in the tubular esophagus can be treated with mucosal ablation. BEST PRACTICE ADVICE 16: Patients should be counseled on cancer risk in the absence of BET, as well as after BET, to allow for informed decision-making between the patient and the physician.

Management strategies for gastroesophageal reflux disease.

In the treatment of gastroesophageal reflux disease (GERD), the most effective treatment option is the use of proton pump inhibitor (PPI), which minimizes the effect of gastric acid on the distal esophagus. Both the step-up and step-down treatment strategies have advantages and disadvantages. Most physicians would like to choose the step-down therapy rather than the step-up therapy. The 'No-step' PPI therapy (i.e. continuous PPI therapy) is another relevant option. After an initial remission, long-term PPI therapy is an appropriate form of maintenance therapy in many patients. As a treatment plan for non-erosive reflux disease, a standard dose of PPI for 4-8 weeks followed by either the step-down strategy or the on-demand treatment strategy is acceptable. When treating erosive esophagitis, PPI is better than H(2) receptor blockers in healing mucosal breaks and relieving symptoms. Long-term maintenance PPI therapy is reported to be very effective in maintaining the remission of reflux esophagitis for up to 5 years. On-demand PPI is also another good option for a maintenance therapy in erosive esophagitis. In Barrett's esophagus, symptoms seem to be well-controlled with PPIs. Unfortunately, however, PPIs have no effect on the shortening of Barrett's esophagus or in preventing the progression to dysplasia and adenocarcinoma. In summary, after reviewing existing guidelines a rather simple guideline on the management of GERD is suggested - PPI should be given for 4-8 weeks followed by either on-demand or maintenance PPI therapy according to the clinical severity.

Esophagus

The gastro-esophageal junction (also known as the esophagogastric junction) is the junction between the esophagus and the stomach, at the lower end of the esophagus. The pink color of the esophageal mucosa contrasts to the deeper red of the gastric mucosa, and the mucosal transition can be seen as an irregular zig-zag line, which is often called the z-line. Histological examination reveals abrupt transition between the stratified squamous epithelium of the esophagus and the simple columnar epithelium of the stomach. Normally, the cardia of the stomach is immediately distal to the z-line and the z-line coincides with the upper limit of the gastric folds of the cardia; however, when the anatomy of the mucosa is distorted in Barrett's esophagus the true gastro-eshophageal junction can be identified by the upper limit of the gastric folds rather than the mucosal transition. The functional location of the lower oesophageal sphincter is generally situated about below the z-line.

Review article: approaches to Barrett's oesophagus treatment-the role of proton pump inhibitors and other interventions.

Despite implementation of screening and surveillance strategies, a significantly large number of patients with Barrett's oesophagus remain undiagnosed. In those who are identified, the management options include acid reduction therapies with proton pump inhibitors or anti-reflux surgery. Endoscopic ablative therapies have also been attempted. In addition to having inherent procedure-related risks with ablative therapies, these alternatives may be limited by high rates of failure, need for continued acid suppressive therapy, metaplasia persistence under otherwise normal appearing tissue, need for procedural expertise, and continued risk for adenocarcinoma development. Therefore, a widely applicable chemoprevention strategy that cost-effectively reduces the rate of progression from oesophagitis to adenocarcinoma in high-risk patients and perhaps those at lower rates of risk is highly desirable. The AspECT trial currently underway is seeking to determine the effects of high- and low-dose proton pump inhibitor therapy with and without low-dose aspirin as Barrett's oesophagus chemoprevention.

Prevalence of Barrett's esophagus by endoscopy and histologic studies: a prospective evaluation of 306 control subjects and 376 patients with symptoms of gastroesophageal reflux.

The classic endoscopic diagnosis of a Barrett's esophagus (BE) is based on the finding of > or =3 cm, of distal esophagus covered by specialized columnar epithelium. However, currently, it is based on the finding of intestinal metaplasia (IM) at the squamous-columnar mucosal junction, independent of its extent. The aim of this study was to determine the prevalence of Barrett's esophagus by endoscopic and histological findings in control subjects and in patients with symptoms of gastroesophageal reflux (GER). Three hundred and six control subjects and 376 patients with symptoms of gastroesophageal reflux were included in this prospective study. Patients with Barrett's esophagus were classified in three groups as follows. 1. Intestinal metaplasia at the cardia. When endoscopy showed non-Barrett's esophagus, but histological intestinal metaplasia was found. 2. Short-segment Barrett's esophagus. When <3 cm, was covered with tongues or finger-like or creeping substitution of distal esophagus. 3. Long-segment Barrett's esophagus. When > 3 cm, of distal esophagus was covered by specialized columnar epithelium. Two biopsies at the antrum, four biopsies at the squamous-columnar junction and one or two at the distal esophagus were taken. In control subjects, 1.6% showed histological IM at the esophagogastric junction. In patients with GER without esophagitis or with erosive esophagitis, IM was found in 18% and 10.7% respectively. 'Short-segment' Barrett's esophagus was three times more frequent than 'long-segment' Barrett's esophagus. Patients with Barrett's esophagus were significantly older than the other groups. The presence of complications or erosions, peptic ulcer or stricture were significantly more frequent among patients with 'long-segment' Barrett's esophagus (p < 0.0001). The prevalence of dysplasia was similar in all groups of patients with Barrett's esophagus. Complications such as ulcers, stricture and dysplasia were exclusively seen among patients with BE, whereas non-Barrett's patients did not exhibit these complications. In control subjects, IM can be found in a low percentage of cases. Among patients with symptoms of GER, the classic endoscopic diagnosis of a Barrett's esophagus can underestimate this condition in 80% of the cases. Patients with intestinal metaplasia at the cardia already present 17% of the cases with low-grade dysplasia. In all patients with symptoms of GER, systematic biopsies at the squamous-columnar junction should be taken.

Recurrence of Barrett's Esophagus is Rare Following Endoscopic Eradication Therapy Coupled With Effective Reflux Control.

Recent data suggest that effective control of gastroesophageal reflux improves outcomes associated with endoscopic eradication therapy (EET) for Barrett's esophagus (BE). However, the impact of reflux control on preventing recurrent intestinal metaplasia and/or dysplasia is unclear. The aims of the study were: (a) to determine the effectiveness and durability of EET under a structured reflux management protocol and (b) to determine the impact of optimizing anti-reflux therapy on achieving complete eradication of intestinal metaplasia (CE-IM). Consecutive BE patients referred for EET were enrolled and managed with a standardized reflux management protocol including twice-daily PPI therapy during eradication. Primary outcomes were rates of CE-IM and IM or dysplasia recurrence. Out of 221 patients enrolled (46.0% with high-grade dysplasia/intramucosal carcinoma, 34.0% with low-grade dysplasia, and 20.0% with non-dysplastic BE) an overall CE-IM of 93% was achieved within 11.6±10.2 months. Forty-eight patients did not achieve CE-IM in 3 sessions. After modification of their reflux management, 45 (93.7%) achieved CE-IM in a mean of 1.1 RFA sessions. Recurrence occurred in 13 patients (IM in 10(4.8%), dysplasia in 3 (1.5%)) during a mean follow-up of 44±18.5 months. The only significant predictor of recurrence was the presence of a hiatal hernia. Recurrence of IM was significantly lower than historical controls (10.9 vs. 4.8%, P=0.04). The current study highlights the importance of reflux control in patients with BE undergoing EET. In this setting, EET has long-term durability with low recurrence rates providing early evidence for extending endoscopic surveillance intervals after EET.

Management of Barrett's esophagus.

In Barrett's esophagus, the squamous lining of the lower esophagus is replaced by columnar epithelium. Barrett's esophagus is associated with gastroesophageal reflux and an increased risk of the development of esophageal cancer. Endoscopy shows red columnar epithelium in the lower esophagus. Biopsy is needed to confirm intestinal metaplasia. Some cases progress from dysplasia to invasive adenocarcinoma. Medical or surgical antireflux treatment controls symptoms and esophagitis, but Barrett's esophagus remains. Patients are usually followed up by endoscopy for detection of dysplasia or early cancer. For patients with low-grade dysplasia, follow-up is adequate; however, for those with high-grade dysplasia, esophagectomy or experimental endoscopic mucosal ablation is advised.

[Endoscopic treatment of Barrett's oesophagus].

Aims of the treatment of Barrett's oesophagus (BO) are disappearance of symptoms and inflammatory complications of gastro-oesophageal reflux disease (GORD), prevention of occurrence of dysplasia and adenocarcinoma, and early treatment of high-grade dysplasia (HGD) and adenocarcinoma. Anti-secretory treatment with proton-pump inhibitors (PPI) must result in disappearance of both symptoms and oesophagitis. The only correction of symptoms, as well as normalization of pHmetry, are not considered as adequate criteria for efficiency of treatment. It has not been demonstrated that treatment with PPI prevented occurrence of dysplasia and adenocarcinoma so the only BO is not an indication for treatment with PPI, which results in only partial regression of height and/or surface of BO. Endoscopic ablation of BO, combined with PPI, allows complete regression of intestinal metaplasia in about 50% of cases. Photodynamic therapy (PDT) seems the best technique for treatment of HGD and mucosal adenocarcinoma. This treatment is not indicated in case of low-grade dysplasia, since its benefit on survival is less clear than for HGD. Endoscopic treatment does not suppress the need for prolonged endoscopic follow-up since BO recurs in approximately one third of patients. For HGD isolated or associated with mucosal adenocarcinoma (proven by endoscopic ultrasound), endoscopic treatment can consist in mucosectomy or ablation with PDT or plasma argon coagulation (PAC) of these lesions if localized, possibly followed by complete ablation of BO by PAC, and always associated with an efficient treatment of GORD by PPI or anti-reflux surgery. Submucosal adenocarcinomas must be treated by oesophagectomy if allowed by the general condition of the patient.

[Endoscopic fluorescence diagnosis of esophageal carcinoma after sensitization with 5-aminolevulinic acid].

Barrett's esophagus is a complication of gastroesophageal reflux disease (GERD) characterized by specialized columnar epithelium that contains goblet cells and replaces the squamous epithelium of the distal esophagus. It is found in about 10% of patients with symptomatic reflux disease and more importantly has been associated with the development of esophageal cancer. Adenocarcinoma arises from dysplasia, which is usually not visible during routine endoscopy, therefore extensive random sampling of the entire Barrett's segment should be performed with biopsies in the 4 quadrants every 1 to 2 cm and of any macroscopic abnormality. We report the history of a 60-year-old man who was admitted to hospital because of an ulcer in Barrett's esophagus not healing despite conservative treatment. He has suffered from gastroesophageal reflux disease for more than 30 years and an antireflux surgical procedure had not resulted in regression of Barrett's esophagus. However, close surveillance could not reveal any dysplastic or malignant lesion. Endoscopic fluorescence detection (EFD) after sensitization with 30 mg/kg 5-aminolevulinic acid (5-ALA) in this patient demonstrated a selective red fluorescence in a macroscopically normal appearing area near the already known ulcer. Biopsies from this fluorescent area showed an adenocarcinoma. Esophagectomy confirmed the presence of intramucosal adenocarcinoma without lymph node metastases.

A novel endoscopic submucosal dissection technique for proton pump inhibitor-refractory gastroesophageal reflux disease.

Although drug treatment is the usual first-line therapy for gastroesophageal reflux disease (GERD), not all patients receive satisfactory relief from drug therapy, alone. We developed an endoscopic fundoplication technique using endoscopic submucosal dissection (ESD); the technique is referred to as ESD for GERD (ESD-G). This study investigated the safety and efficacy of this novel technique in patients with drug-refractory GERD. ESD-G narrows the hiatal opening through ESD of the esophagogastric junction (EGJ) mucosa. For safety reasons, the range of mucosal resection was limited to half (1/2 or 1/4 +1/4) of the circumference of the EGJ lumen. ESD-G was performed on 13 patients with proton pump inhibitor (PPI)-refractory GERD. GERD symptoms, PPI dose, and 24-h esophageal pH monitoring results were compared before and 6 months after the procedure. Results. In 12 cases, symptoms significantly improved after ESD-G. Five patients demonstrated improved esophagitis, three were able to discontinue PPI therapy, and three were able to reduce their PPI dosage following surgery. The esophageal pH <4 holding time ratio was also decreased after ESD-G. Conclusions. ESD-G may be useful for PPI-refractory GERD patients.

Barrett's esophagus.

Barrett's esophagus denotes the presence of columnar epithelium in the esophagus instead of the usual stratified squamous epithelium. Barrett's esophagus had been thought to represent a mediastinal extension of the stomach in patients with a congenital short esophagus. Subsequent clinical and experimental data have established the abnormality as an acquired condition resulting from chronic gastroesophageal reflux. Although roentgenographic studies may show a mild-esophageal stricture or an esophageal ulcer, definitive diagnosis requires endoscopy with directed biopsy of erythematous mucosa in the esophagus, or manometrically guided biopsies for showing the presence of columnar epithelium above the lower esophageal sphincter. Although the origin of the cells causing this epithelium is still unclear, three distinct epithelial types have been found: atrophic gastric-fundic, junctional, and specialized columnar. Esophageal strictures and esophageal ulcers are complications associated with Barrett's esophagus, but its major significance is the association with the development of adenocarcinoma of the esophagus. Treatment of Barrett's esophagus is aimed at preventing gastroesophageal reflux with the additional need for close endoscopic surveillance for the development of dysplasia or early adenocarcinoma. Whether the diagnosis of Barrett's esophagus mandates anti-reflux surgery (fundoplication) remains controversial.

Overlap of reflux and eosinophilic esophagitis in two patients requiring different therapies: a review of the literature.

Eosinophilic esophagitis (EE) and gastroesophageal reflux disease (GERD) have overlapping clinical, manometric, endoscopic and histopathologic features. The diagnosis of EE is nowadays based upon the presence of 15 or more eosinophils per high power field (eo/HPF) in esophageal biopsies. We report the cases of two young males suffering from dysphagia and recurrent food impaction with reflux esophagitis and more than 20 eo/HPF in upper-mid esophagus biopsies, both of which became asymptomatic on proton pump inhibitor (PPI) therapy. The first patient also achieved a histologic response, while EE remained in the other patient after effective PPI treatment, as shown by 24-h esophageal pH monitoring. Topical steroid therapy combined with PPI led to complete remission in this latter patient. GERD and EE may be undistinguishable, even by histology, so diagnosis of EE should only be established after a careful correlation of clinical, endoscopic and pathologic data obtained under vigorous acid suppression. These diagnostic difficulties are maximal when both diseases overlap. Limited data are available about this topic, and the interaction between EE and GERD is a matter of debate. In this setting, upper-mid esophagus step biopsies and esophageal pH monitoring of patients on PPI therapy are pivotal to evaluate the role of each disease. A PPI trial is mandatory in patients with a histopathologic diagnosis of EE; in those unresponsive to PPI treatment, EE should be suggested. However, a clinical response to PPI may not rule out quiescent EE, as shown in this report.

Laparoscopic transgastric esophageal mucosal resection for high-grade dysplasia.

High-grade dysplasia of the esophageal mucosa has been shown to be a precursor to adenocarcinoma. In addition to esophagectomy, multiple ablative endoscopic techniques have evolved for the management of this condition. As a surgical alternative to esophagectomy, we describe for the first time a new option in the treatment of high-grade dysplasia. Two patients with a history of gastroesophageal reflux disease (GERD) underwent upper gastrointestinal endoscopy which demonstrated high-grade dysplasia of the distal esophagus. The first patient had a short segment (0.5-1.0 cm), and the second patient had a longer (2 cm) segment of dysplasia. The patient is placed in the modified lithotomy position. Five trocars are placed as if to perform a fundoplication. A complete circumferential mobilization of the esophagus is performed. The short gastric vessels are divided with the harmonic scalpel, to free up the fundus of the stomach. An anterior horizontal gastrotomy is performed three to four centimeters below the gastroesophageal junction. A solution of epinephrine and normal saline (1:100,000) is injected into the mucosa at the Z-line and, utilizing specially designed hook electrocautery, the mucosa is incised circumferentially around a lighted bougie. Using blunt dissection the mucosa is undermined, elevated, and excised in four quadrants. Three centimeters of the distal esophageal mucosa are resected. The gastrotomy is then closed using a linear stapler, and a 360 degrees fundoplication is performed around a 50 Fr bougie. High-grade dysplasia was identified in the specimens from both patients; however, neither patient was found to have carcinoma in situ or invasive esophageal cancer. Our first patient has been followed for twenty months, the second for ten months. Both patients underwent routine upper gastrointestinal endoscopy for surveillance of the healing process. At eight months, the mucosa of the first patient showed complete regeneration of squamous epithelium. Our most recent patient appears to be progressing without complications and has also demonstrated normal squamous epithelium at ten months postoperatively, without changes of Barrett's epithelium. The technique of laparoscopic transgastric esophageal mucosal resection is feasible and may be proven to be an alternative to esophagectomy for the management of high-grade dysplasia.

[Oesophageal diseases: gastroesophageal reflux disease, Barrett's disease, achalasia and eosinophilic oesophagitis].

The most important novel findings presented on oesophageal disease in DDW 2015 were the following: 1) GERD: a) hypervigilance seems to be a key pathogenic factor in reflux symptoms refractory to PPI; b) post-reflux swallowing-induced peristaltic waves could be an excellent diagnostic criterion for GERD; c) laryngeal pH-metry is not useful in the diagnosis of extra-oesophageal symptoms; d) the recommendation of weight loss adequately recorded in the clinical reports of patients with GERD and obesity or overweight is an excellent quality indicator and is associated with better outcomes. 2) Barrett's oesophagus: a) persistent low-grade dysplasia in more than one endoscopy and a diagnosis of "indefinite for dysplasia" are associated with a high risk of neoplastic progression; b) narrow-band imaging allows areas of dysplasia on Barrett's oesophagus to be identified with high sensitivity and specificity; c) initial endoscopy fails to identify a high percentage of advanced neoplasms in Barrett's oesophagus. Early re-endoscopy should be considered; d) endoscopists specialized in Barret's oesophagus obtain a much higher yield in the diagnosis of advanced lesions. Patients at high risk-men, older patients, smokers and those with long-segment Barrett's oesophagus-could benefit from follow-up in a referral center. 3) Achalasia: POEM seems safe and effective, independently from patient characteristics (age, comorbidity) and the technical variations used. 4) Eosinophilic esophagitis: topical budesonide and exclusion diets are reasonably effective in PPI non-responders.

Endoscopic management of Barrett's esophagus: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement.

Current practices for the management of Barrett's esophagus (BE) vary across Europe, as several national European guidelines exist. This Position Statement from the European Society of Gastrointestinal Endoscopy (ESGE) is an attempt to homogenize recommendations and, hence, patient management according to the best scientific evidence and other considerations (e.g. health policy). A Working Group developed consensus statements, using the existing national guidelines as a starting point and considering new evidence in the literature. The Position Statement wishes to contribute to a more cost-effective approach to the care of patients with BE by reducing the number of surveillance endoscopies for patients with a low risk of malignant progression and centralizing care in expert centers for those with high progression rates.Main statements <bMS1</b The diagnosis of BE is made if the distal esophagus is lined with columnar epithelium with a minimum length of 1 cm (tongues or circular) containing specialized intestinal metaplasia at histopathological examination. <bMS2</b The ESGE recommends varying surveillance intervals for different BE lengths. For patients with an irregular Z-line/columnar-lined esophagus of < 1 cm, no routine biopsies or endoscopic surveillance is advised. For BE ≥ 1 cm and < 3 cm, BE surveillance should be repeated every 5 years. For BE ≥ 3 cm and < 10 cm, the interval for endoscopic surveillance should be 3 years. Patients with BE with a maximum extent ≥ 10 cm should be referred to a BE expert center for surveillance endoscopies. Patients with limited life expectancy and advanced age should be discharged from endoscopic surveillance. <bMS3</b The diagnosis of any degree of dysplasia (including "indefinite for dysplasia") in BE requires confirmation by an expert gastrointestinal pathologist. <bMS4</b Patients with visible lesions in BE diagnosed as dysplasia or early cancer should be referred to a BE expert center. All visible abnormalities, regardless of the degree of dysplasia, should be removed by means of endoscopic resection techniques in order to obtain optimal histopathological staging <bMS5</b All patients with a BE ≥ 10 cm, a confirmed diagnosis of low grade dysplasia, high grade dysplasia (HGD), or early cancer should be referred to a BE expert center for surveillance and/or treatment. BE expert centers should meet the following criteria: annual case load of ≥10 new patients undergoing endoscopic treatment for HGD or early carcinoma per BE expert endoscopist; endoscopic and histological care provided by endoscopists and pathologists who have followed additional training; at least 30 supervised endoscopic resection and 30 endoscopic ablation procedures to acquire competence in technical skills, management pathways, and complications; multidisciplinary meetings with gastroenterologists, surgeons, oncologists, and pathologists to discuss patients with Barrett's neoplasia; access to experienced esophageal surgery; and all BE patients registered prospectively in a database.