Evidence Of Intestinal Metaplasia Research Articles

S3579 Collagenous Gastritis in a Young, Healthy Patient on an SSRI: A Potential Pharmacologic Link to a Zebra Diagnosis

Introduction: Collagenous gastritis is a rare disease primarily affecting the digestive system characterized by thick subepithelial collagen bands ( >10 μm) associated with an inflammatory infiltrate of the gastric mucosa. Since it was first reported in 1989, less than 100 cases have been documented in English literature. With fewer than 100 reported cases and no established etiology, no standard therapy exists based on randomized, controlled clinical trials. The objective of this case report is to add to the current knowledge on collagenous gastritis by proposing the need for further work to evaluate a potential pharmacologic link between SSRI use and the disease. Case Description/Methods: A healthy 25 year old woman a past medical history of generalized anxiety disorder (on longstanding Sertraline) presented for evaluation of several months of generalized abdominal discomfort, frequent eructation, nausea, and bloating. She denied any other gastrointestinal symptoms. The only medication she took regularly was Sertraline 25 mg daily, which she reported taking for at least a year. She did not take nSAIDs, herbal supplements, or vitamins. Physical examination was benign. CBC, CMP, and thyroid function were normal. Serological screening for celiac disease was negative Upper endoscopy demonstrated a normal appearing esophagus, stomach, and small intestine. Biopsies were taken from the antrum, body, and second portion of the duodenum. Gastric biopsies demonstrated collagenous gastritis without evidence of intestinal metaplasia or H. pylori. Duodenal biopsies were normal. The histologic diagnosis was confirmed at Cleveland Clinic. (Figure) Discussion: The ability of antidepressants to affect the immune system in various ways has been studied extensively. For example, one meta-analysis published in 2015 suggested that serum levels of TNF-alpha and IL-6 significantly decreased while no significant change in CRP concentration before and after treatment was observed. Another meta-analysis of 22 studies showed that the level of IL1-Beta in patient's serum significantly decreased, IL-6 slightly decreased, TNF-alpha levels did not change regardless of taken medication (SSRI, SNRI, or TCA). We propose that the development of this patient's collagenous gastritis was mediated by her use of sertraline, perhaps through downregulation of TNF-alpha and IL-6, known proinflammatory cytokines. Further studies are needed to test this hypothesis.Figure 1.: Actual endoscopic images of patient’s stomach: A. cardia B. fundus C. antrum.

S2257 Cirrhosis, Varices, and Barrett’s Esophagus: WATS3D-only Surveillance and Band Ligation in the Management of Nondysplastic Barrett’s Esophagus Progressing to High Grade Dysplasia With Underlying Esophageal Varices

Introduction: Wide-area transepithelial sampling with 3-dimensional computer-assisted analysis (WATS3D) is an emerging technique used to collect esophageal samples via transepithelial brushing. WATS3D can be a safe and useful tool in Barrett’s esophagus (BE) management in patients with underlying small esophageal varices (EV) where traditional 4 quadrant cold forceps biopsies (CFB) would be contraindicated due to the risk of adverse events such as bleeding. We describe the utility of WATS3D-only surveillance combined with band ligation in the management and eradication of BE which progressed to high grade dysplasia (HGD) in a patient with underlying cirrhosis and EV. Case Description/Methods: We present a 66-year-old male with a history of nondysplastic (ND) BE (C0-M1), small Grade 1 EV and cirrhosis who presented for BE surveillance. Due to underlying EV and associated risk of bleeding, CFB was not performed and sampling with WATS3D-only was undertaken. WATS3D was first performed with surveillance esophagogastroduodenoscopy (EGD) in 2015 and demonstrated ND BE. On further EGD surveillance, BE histology remained ND until early 2021 where WATS3D revealed low grade dysplasia (LGD). Repeat EGD with WATS3D brushing was performed 4 months later, which demonstrated progression to HGD. Interval surveillance EGD with WATS3D brushing was, again, performed 4 months later and demonstrated LGD with rare foci of HGD. Of note, in both instances band ligation of the dysplastic segments was done. EGD with WATS3D 3 months later revealed endoscopic clearance of BE post-banding and pathology report revealed, ND, non-goblet cell metaplasia. The final interval surveillance EGD with WATS3D, 3 months later, showed complete eradication of BE with no evidence of intestinal metaplasia. Table 1 provides a thorough chronological description from first EGD to complete resolution of BE, 8 years later. Discussion: WATS3D has been increasingly shown to be an effective BE surveillance and screening tool. However, given the lack of data regarding appropriate surveillance windows for WATS3D-only BE surveillance, we performed sampling at shorter intervals than what would otherwise be recommended, to confirm the lack of dysplasia. This case presents a unique approach to WATS3D-only surveillance combined with band ligation therapy of dysplasia in the management of BE in a cirrhotic patient with underlying EV. Additionally, this case is unique in clearly documenting progression of a short segment of ND BE to HGD with WATS3D sampling alone. Table 1. - Summary of findings and intervention from first EGD to complete resolution of BE (8 year window) Date Variceal Grade Prague Score Number of BE Islands Sampling done by WATS3D Pathology Findings Banding therapy (# of bands) 04/09/14 2 C0-M1 3 No N/A 0 07/29/15 2 C0-M1 Scattered No N/A 0 12/2315 1 C0-M1 Scattered Yes No dysplasia 0 06/15/16 1 C0-M1 Scattered Yes No dysplasia 0 02/08/17 2 C0-M1 Scattered No N/A 4 01/22/18 1 C0-M1 1 No N/A 0 01/30/19 2 C0-M1 2 No N/A 0 01/29/20 1 C0-M1 2 No N/A 0 02/01/21 1 C0-M1 2 Yes Low-grade dysplasia 0 06/01/21 1 C0-M1 2 Yes High-grade dysplasia 3 10/25/21 1 C0-M1 2 Yes Low-grade with rare foci of high-grade dysplasia 2 01/25/22 1 N/A 3 Yes Non-goblet cell metaplasia, no dysplasia 0 04/25/22 1 N/A 0 Yes Squamocolumnar, no dysplasia or metaplasia 0

Prognostic Impact of the Presence of Barrett's Esophagus and Intestinal Metaplasia on Esophageal Adenocarcinoma Survival.

Barrett's esophagus (BE), defined by the presence of intestinal metaplasia (IM) on histology, is thought to be the only identifiable precursor lesion for esophageal adenocarcinoma (EAC). Recent studies have suggested the possibility of an alternate, non-IM associated EAC that is a more aggressive form of EAC with worse survival. Among EAC patients, we aimed to compare survival of patients with and without IM at the time of diagnosis. This was a retrospective cohort study of all patients with histologic confirmed EAC evaluated at a tertiary care center from 2013 to 2019. Cases were categorized according to the presence or absence of IM on histologic specimens (Group I-IM-EAC and Group II-non-IM-EAC). We compared demographic characteristics, clinical stage, therapy, and survival between the 2 groups using the Chi-square and ANOVA tests (for categorical and continuous variables, respectively). We used Cox proportional hazards regression to determine the association of IM with overall survival, adjusting for sex, age at diagnosis, tumor location, histologic grade, and clinical stage. A total of 475 patients were included in this analysis (mean age 64.8 years [SD 10.8], 89% white) and 109 (23.0%) had no evidence of IM. Compared with IM-EAC (Group I), individuals in the non-IM-EAC group were younger (P = .01) and had a greater proportion of patients diagnosed with advanced disease (49.5 vs 20.2% for stage 4, P < .001). These patients were less likely to undergo endoscopic therapy alone (0.92% vs 29.78%, P < .001) or surgery alone (0 vs 9.84%, P = .001). On multivariable analysis, the presence of IM-EAC was associated with improved overall survival compared to non-IM-EAC (HR 0.69, 95% CI 0.49-0.96). Additional factors associated with poor survival was increasing stage of diagnosis (HR 6.49: 95% CI 3.77-11.15 for stage 4, HR 2.19: 95% CI 1.25-3.84 for stage 3, HR 2.04: 95% CI 0.98-4.25 for stage 2 compared to stage 1) and more advanced histologic stage (HR 2.00, 95% CI 1.26-3.19) for poorly/undifferentiated compared to well differentiated). EAC without the presence of IM on histology was associated with worse survival compared to those with IM. Future prospective studies with detailed molecular sequencing are required to clarify if 2 separate phenotypes of EAC exist (IM-EAC and non-IM-EAC). If confirmed, this may have significant implications for screening and management strategies.

S1927 Collagenous Gastritis With Esophageal Involvement: An Unusual Cause of Dysphagia

INTRODUCTION: Collagenous gastritis is characterized by thickened superficial subepithelial collagen layer in the gastric mucosa. To date, about 60 cases of collagenous gastritis have been described in the literature. Cases have been divided into two phenotypes: pediatric patients who typically present with abdominal pain and anemia and adult patients who typically present with diffuse diarrhea and gastrointestinal tract involvement. However, only one case has documented collagenous involvement of the esophagus. Currently, there is no established standard therapy for this condition, however several medications including anti-secretory agents and steroids have been used with varying success. We present an unusual case of an adult who presents with dysphagia and was found to have collagenous gastritis with esophageal involvement. CASE DESCRIPTION/METHODS: A 45-year-old female with a history of Dieulafoy lesion status post partial gastrectomy at age 18 presented to clinic with dysphagia. The patient reported 6 months of difficulty swallowing solid food and gastroesophageal reflux for which she was taking ranitidine as needed. On physical exam, she was afebrile and hemodynamically stable with a soft, non-tender abdomen. Esophagogastroduodenoscopy (EGD) was notable for a normal endoscopic appearance of the esophagus and pale mucosa with scattered plaque-like lesions throughout the gastric body. Esophageal biopsies demonstrated squamocolumnar mucosa with a patchy thickened subepithelial collagen plate in the columnar component. Separate biopsies of the pale mucosa and plaques in the gastric body revealed histopathologic features consistent with collagenous gastritis and no evidence of intestinal metaplasia, dysplasia or Helicobacter pylori. Serum tissue transglutaminase IgA and intrinsic factor antibody were non-contributory. She was started on a proton pump inhibitor twice daily and reported symptomatic improvement at six-month follow-up. Histopathology of biopsies obtained during a repeat EGD at six-month follow-up demonstrated resolution of the subepithelial collagen plate previously seen in the esophagus and gastric body. DISCUSSION: Esophageal involvement of collagenous gastritis resulting in dysphagia is an unusual presentation of a rare disease. Although prior reports have described two distinct subsets of the disease, additional cases are important to better characterize the disease and guide management.Image 1.: Histopathological findings of distal esophageal biopsies. (A) (H&E stain, 100x magnification) showing pink, thickened subepithelial collagen plate (arrow) and overlying epithelium with focal erosion, both characteristic features of collagenous gastritis. (B) (Trichrome stain, 100x magnification) highlighting the thickened subepithelial collagen plate in blue (arrow).Image 2.: Histopathological findings of the gastric fundus biopsies. (A) (Trichrome stain, 400x magnification) highlighting the thickened subepithelial collagen plate in light blue (arrow). The collagen plate measures >100 um at its thickest point, well above the cut off of 10 um typically used to diagnose collagenous gastritis. In addition, the collagen can be seen entrapping the surrounding inflammatory cells and blood vessels, another key histologic feature of collagenous gastritis. (B) One of the atrophic appearing areas on endoscopy (H&E stain, 100x magnification) showing chronic atrophic gastritis with complete loss of parietal and chief cells. There is also prominent pseudo pyloric metaplasia but no evidence of intestinal metaplasia or H. pylori. These features are also consistent with diagnosis of collagenous gastritis.Image 3.: Endoscopic findings of the gastric body. Numerous plaque-like lesions were scattered throughout the gastric body interspersed with atrophic-appearing mucosa.

S2920 Oxyntic Gland Adenoma of the Stomach; A Case Study of an Under-Reported Entity

INTRODUCTION: Oxyntic gland adenoma (OGA), also known as gastric adenocarcinoma with chief cell predominance is a rare entity, with incidence and prevalence data unknown. Given its rarity, we present a case of OGA incidentally found on EGD in a patient with complaints of dyspepsia. CASE DESCRIPTION/METHODS: A 58-year-old female with a history of smoking presented to the GI clinic for colorectal cancer screening. On presentation, ROS was only notable for dyspepsia not related to food intake or exercise. Her physical exam was unremarkable. She was scheduled for both colonoscopy for cancer screening and EGD for evaluation of dyspepsia. Colonoscopy was negative for cancer. EGD showed a solitary papule in the gastric fundus (Figure 1). The papule was raised, pale/white in color, 4 mm in diameter, and had a highly vascularized base. The papule was completely excised with cold biopsy forceps. Pathological analysis was notable for a completely resected papule without evidence of intestinal metaplasia. Further analysis revealed that the papule was composed of fundic gland mucosa, with chief cells predominating and low-grade cytologic features consistent with an oxyntic gland adenoma (Figures 2 and 3). DISCUSSION: OGA is characterized as a benign, solitary, polypoid growth, usually located in the fundus and less often in the cardia of the stomach. Prior studies have explored the histological patterns of these polyps and have defined them as either chief cell predominant, or a mixture of chief and parietal cells. The nomenclature is disputed as multiple names have been proposed for a similar histological description including: chief cell hyperplasia, chief cell hamartoma, and oxyntic gland adenocarcinoma with chief cell predominance. The last is a misnomer as these polyps lack atypical features such as mucous gland cells or foveolar epithelium. Additionally, they do not invade through the submucosa, as seen in other carcinomas. As some pathologists and gastroenterologists are still unfamiliar with the clinical and histological presentation of OGA, we highlight this rare finding for further discussion of its proper nomenclature and a better understanding of etiology, incidence, and prevalence in the United States.Figure 1.: Endoscopic View of Polyp (Encompassed in Black Circle).Figure 2.: Full Slice of Polyp revealing Fundic Type Mucosa Containing Oxyntic Gland Adenoma.Figure 3.: 200x Zoomed view of Fundic Mucosa with Oxyntic Gland Adenoma (Black Arrow points to normal Oxyntic gland and White arrows point to Oxyntic gland with Chief cell predominance).

3124 Endoscopy in Patient With Situs Inversus Totalis

INTRODUCTION: Situs inversus totalis (SIT) is the complete transposition of the abdominal and thoracic organs. Due to the inherent anatomic differences, patients with situs inversus may pose a unique challenge when undergoing endoscopic procedures because physicians are trained to maneuver the endoscope in a certain manner. CASE DESCRIPTION/METHODS: A 51 year old male presents with a 3 year history of intermittent rectal bleeding. He denies abdominal pain, constipation, and diarrhea. On presentation, physical exam was normal. Although the patient was aware of his diagnosis of SIT at the time of endoscopy, he did not think it was necessary to inform physicians about his condition. In addition, multiple electrocardiograms had been read previously without complications. Laboratory evaluations were normal except for slightly elevated ALT and AST. EGD was performed and showed salmon-colored mucosa in the distal esophagus. Biopsies of the esophagus showed squamous epithelium with acute inflammation and reflux-associated changes, and no evidence of intestinal metaplasia. The stomach was diffusely erythematous and biopsies revealed chronic active gastritis with H. pylori-like organisms. Colonoscopy was normal with the exception of internal hemorrhoids. EGD and colonoscopy were both successfully performed in the standard manner. SIT was discovered during a liver ultrasound performed to further investigate the etiology of his elevated liver function tests. DISCUSSION: Situs inversus totalis may cause additional challenges for endoscopists. One study found that SIT prolonged cecal intubation times. Certain modifications to standard endoscopic technique have been proposed including turning the endoscope 180 degrees clockwise first in the stomach then again in the duodenum, as well as placing the patient in the right lateral decubitus position so that the maneuvers are performed inversely. In our case, the endoscopist was able to successfully navigate the endoscopic procedures without special maneuvers or changes in position and was unaware of the diagnosis of SIT until after the procedure. In conclusion, endoscopies and colonoscopies are feasible in patients with SIT. Various modifications to the endoscopic technique have been suggested, but may not always be required, to safely perform these procedures on patients with SIT.

1784 Esophageal Granular Cell Tumor Treated With Cap-Assisted Endoscopic Mucosal Resection

INTRODUCTION: Granular cell tumors (GCT) are rare neoplasms that can occur throughout the body. They were first described in the tongue by Abrikossoff in 1926 and initially known as Abrikossoff tumor. Most GCTs are benign neoplasms with a schwann cell origin however they may also be locally aggressive. CASE DESCRIPTION/METHODS: We encountered a 38 years-old Female with no past medical history who underwent gastroscopy for non-specific abdominal pain. She was incidentally found to have a 1 cm, oval, submucosal lesion at 29 cm from the incisors (Figure 1). Endoscopic ultrasound (EUS) was pursued and revealed a hyperechoic lesion that appeared to be located within the luminal interface/superficial mucosa (Figure 2). The mass measured 8 mm in maximal thickness on EUS. Cap-assisted endoscopic mucosal resection was planned. A solution of saline and methylene blue was injected with the adequate lifting of the lesion from the underlying muscularis propria. A distally attaching cap was fitted with a snare in anticipation of endoscopic mucosal resection (EMR). The lesion and a peripheral margin (total area of 18 mm) were successfully resected and retrieved by suctioning into the cap (Figure 3). Pathology of the specimen showed a granular cell tumor with affirmative S100 and no evidence of intestinal metaplasia or dysplasia. Surveillance EGD, performed 3 months after the initial EMR, confirmed complete resection with no recurrence. Biopsies revealed benign esophageal squamous mucosa. DISCUSSION: Cap-assisted EMR is a valuable tool in the armamentarium of the gastroenterologist. It offers the benefits of EMR, in that this technique is able to obtain larger tissue samples compared to biopsy without the loss of a safety profile and provides the added pleasantry of a short learning curve. It is limited by the size of the cap and is unable to resect more extensive lesions en-bloc. Lesions smaller than 3 cm in diameter that is confined to mucosal or submucosal layers are the ideal candidates for this technique, as evidenced by our case.

482 NEW QUALITY MEASURES FOR ENDOSCOPIC ERADICATION THERAPY IN BARRETT’S ESOPHAGUS: IS 18 MONTHS AN APPROPRIATE TARGET TO ACHIEVE COMPLETE ERADICATION?

The ASGE and ACG recently published proposed quality measures for endoscopic eradication therapy (EET) for Barrett’s esophagus (BE). Many of these measures were based on expert opinion rather than evidence of improved patient outcomes. One particular measure suggested that complete eradication of intestinal metaplasia (CE-IM) should be achieved in 70% of patients within 18 months of initiating EET. The purpose of this study was to assess whether an 18-month timeline to achieve this endpoint is associated with improved long-term clinical outcomes. A retrospective single-center cohort study was performed of patients who underwent EET for BE between 2006 and 2017. Patients were included in analyses if CE-IM had been achieved or if CE-IM had not been achieved and an endoscopy had been performed at least 18 months since initiating EET. Data on patient characteristics, baseline BE histology, BE length, and hiatal hernia size were recorded. Treatment received, complications, and follow up data were recorded, including recurrence and progression dates, locations, and histology. CE-IM was defined as a single endoscopy after initiation of EET that demonstrated no endoscopic evidence of BE and no evidence of intestinal metaplasia on biopsies. Proportions and means or medians were calculated to summarize data. The Kaplan-Meier method was used to compare recurrence rates. Multivariable Cox proportional hazards modeling was used to identify predictors of recurrence. A total of 291 BE patients were treated with EET, had sufficient follow-up, and were included in the analyses. (TABLE) The majority (74.2%) had baseline histology of high-grade dysplasia (HGD) or intramucosal adenocarcinoma. CE-IM was achieved in 86.3% of patients, with a median time to CE-IM of 13.0 months (IQR 7.9-22.1), and required a median of 3 treatments (IQR 2-5). Only 68.9% of patients who achieved CE-IM did so within 18 months. Less severe baseline histology and shorter BE length were predictors of achieving CE-IM within 18 months. The median follow-up time after CE-IM was 34.2 months (IQR 12.6-63.2). Comparing those who achieved CE-IM within 18 months to those with longer time to CE-IM, there were no differences in the rate of recurrence of IM (log-rank p=0.29) or dysplasia (log-rank p=0.79) (FIGURE), even after adjusting for potential confounders. At the end of follow-up, among patients who achieved CE-IM, four (5.5%) had HGD or cancer; all of these subjects had achieved CE-IM within 18 months. There is no evidence that an 18-month cutoff to achieve CE-IM in BE patients undergoing EET is associated with improved long-term outcomes. Consideration should be given to modifying proposed quality measures for EET in BE based on outcomes data.Tabled 1Characteristics of BE patients who underwent EETTotal291Age, mean63.9 yrs (SD 10.5)Male sex233 (80.1%)White race252 (86.6%)BE length, median (cm)3 cm (IQR 1-5)Hiatal hernia size, median (cm)2 cm (IQR 1-3)Baseline Histology:No dysplasia25 (8.6%)Indefinite for dysplasia9 (3.1%)Low grade dysplasia41 (14.1%)High grade dysplasia161 (55.3%)Intramucosal EAC55 (18.9%) Open table in a new tab

A Retrospective Study Evaluating the Association of Gastric Intestinal Metaplasia and Serum Vitamin D Levels in an Urban Medical Center

Introduction: Recent studies suggest that there is an association between gastric adenocarcinoma and low serum vitamin D levels. However, to date, there are no studies in the literature that have investigated the relationship between the premalignant stages of gastric adenocarcinoma such as intestinal metaplasia and low serum vitamin D levels. Methods: A retrospective, randomized and matched case-control study was conducted with cases defined as subjects who had intestinal metaplasia identified by gastric biopsy and the controls classified as subjects who did not have intestinal metaplasia detected by biopsy and were therefore healthy. All subjects who were included were older than 18 years old, had underwent EGD and had a documented serum 25-hydroxyvitamin D level prior to EGD without repletion. Subjects that were excluded included those who were younger than 18 years old, did not undergo EGD, subjects who did not have a documented Vitamin D level prior to EGD, or if the patient had prior gastrectomy, gastric ulcers, adenomatous polyps, intestinal metaplasia of the esophagus or malignancy including gastric cancer. The cases and control subjects were matched according to age, gender, ethnicity, Body Mass Index (BMI), and H. Pylori infection. A normal serum 25-hydroxyvitamin D level was defined as 30-100 ng/dL. Hypovitamonosis D was divided into two groups based on severity: Vitamin D insufficiency (VDi) and Vitamin D deficiency (VDd). A serum 25-hydroxyvitamin D level that was 20 ng/dL or greater but less than 30 ng/dL was considered VDi in contrast with VDd that was defined as a level less than 20 ng/dL. The mean and standard deviation of the matched patients' age, 25-hydroxyvitamin D level, BMI were calculated. The odds ratio was calculated to assess the association between 25-hydroxyvitamin D levels and Gastric Intestinal Metaplasia with statistical significance defined as a p-value < 0.05. Results: 906 subjects were recruited for this study and 324 subjects met the inclusion criteria. After matching, 168 subjects were included in the final analysis; 84 cases and controls each. The case and control subjects were similar in regards to age, gender, ethnicity, and BMI; most subjects were female (63.1%), Hispanic (77.4%), overweight, and did not have H. Pylori infection (75%). The average serum 25-hydroxyvitamin D level was lower in the Intestinal Metaplasia group (21.88 ng/dL) in comparison with patients who did not have evidence of Intestinal Metaplasia 32.26 ng/dL). Hypovitaminosis D was more common in patients with Intestinal Metaplasia (OR 12.6). Most patients with Intestinal Metaplasia who were found to have hypovitamosis D were more likely to have VDi (OR 78.76) than VDd (OR 34.61). All results had a p-value < 0.01. Conclusion: Although the development of intestinal metaplasia is multifactorial, hypovitaminosis D may contribute as a treatable risk factor.Table: Table. Demographic Information

An Unusual Location for Pancreatic Heterotopia: The Gastroesophageal Junction

: Heterotopic pancreas (HP) is defined as pancreatic tissue found outside the pancreas. When symptoms appear, they are often due to inflammation, obstruction, and malignant transformation. The most common location is the stomach, especially the antrum. HP in the esophagus is uncommon, with only a handful of cases reported in pediatric patients. It rarely occurs in the adult population.We present an atypical case of HP at the gastroesophageal junction (GE) in a middleaged female. Case: A 59 year old African American female was referred for iron deficiency anemia. Patient had recurrent cough. She denied symptoms of dyspepsia. Physical exam was unremarkable. The white blood cell was 9.7 (3.8-10.6), blood Hg 11.9 g/dL, HCT 34.4% with an MCV of 77.8 L, and platelet count was 246. Stool occult testing negative. An esophagogastroduodenoscopy revealed a small, broad-based polyp about 3-4 mm in diameter without umbilication, or evidence of bleeding (Figure 1). It was glimpsed at the GE junction on introduction of the endoscope, and confirmed on a retroflexed view (Figure 2). A biopsy of the polyp was obtained with cold forceps, and sent for histopathologic examination which revealed focal pancreatic acinar cell metaplasia/heterotopia completely surrounded by gastric cardia-type mucosa with chronic active gastritis, acute cryptitis (Figure 3). There was no evidence of intestinal metaplasia or dysplasia, or esophageal squamous mucosa. Because the polyp was located at the GE junction, the origin could have been esophageal or gastric. However, because the surrounding tissue histologically was entirely gastric, a diagnosis of HP of the stomach at the GE junction was assigned. The patient had been asymptomatic and did not present with complications, a follow up plan for endoscopic surveillance was proposed.Figure 1Figure 2Figure 3Discussion: The incidence of HP cases has been reported to be 2 to 15%, with the majority found incidentally during surgery or post-mortem autopsies. Endoscopically, HPs grossly appear as firm white to yellow lobulated nodules and range in size almost 0.2 to 4 cm. Our case was unusual in that it did not have the characteristic umbilication, nor discoloration, but rather a nodular polypoid appearance, and was located not in the atrum or body, but at the GE junction. In a symptomatic patient, resection is performed after other causes are ruled out. In an asymptomatic patient, with benign gross and histological features, lesions are managed conservatively.

Pathogenesis of Barrett s Esophagus

Barrett’s esophagus (BE) is characterized as histologic evidence of intestinal metaplasia is present in distal esophageal epithelium and is an important pathology because it is the major risk factor for developing esophageal adenocarcinoma (EAC). It’s well known that chronic gastroesophageal reflux disease (GERD) leads to the development of metaplasia. However, the cellular and molecular mechanism of the replacement of squamous esophageal epithelium with a columnar type is largely unknown. Efforts to understand the pathogenesis of BE and its disposition to EAC have been increasing over the previous 2 decades. This review aims to explore current data on the major risk factors, origin, genetic changes of BE, provide an insight into the molecular biomarkers related with BE and seek for possible development of therapies that could prevent BE from progressing to EAC.

Endoscopic surveillance of gastrointestinal premalignant lesions: current knowledge and future directions.

Provide an evidence-based resource for the surveillance of gastrointestinal premalignant lesions, focusing on the scientific articles reported recently. No randomized controlled clinical trials exist to definitively support the efficacy of surveillance programs for Barrett's esophagus and gastric intestinal metaplasia. However, surveillance of these premalignant lesions is recommended by some of the leading organizations. To optimize the usefulness of surveillance programs, targeting high-risk patients might maximize its benefits. A Barrett's esophagus segment of at least 3 cm and evidence of intestinal metaplasia can help stratify those patients at highest risk for progression to esophageal adenocarcinoma. The location, extent, and severity of intestinal metaplasia are indicators of risk of developing gastric cancer. Patients with extensive intestinal metaplasia should be offered endoscopic surveillance. Quality in the baseline colonoscopy is crucial to decrease the risk of interval colorectal cancers. The importance of serrated polyps, as well as their surveillance intervals, is emphasized. To optimize the usefulness of surveillance programs, targeting high-risk patients might maximize its benefits. Future research is needed to design more effective surveillance strategies. Recently, emerging imaging techniques hold promise for improving sensitivity of endoscopic surveillance of premalignant conditions in the gastrointestinal tract.

Update zum Barrett-Ösophagus und Barrett-Karzinom

The definition of Barrett esophagus is currently under discussion. It is now suggested that a distal esophagus coated with cylinder epithelium with cardia-fundus mucosa should also be classified as Barrett esophagus because the risk of cancer is significantly increased even without histological evidence of intestinal metaplasia with goblet cells. The results of recent epidemiological investigations imply that the cancer risk of cylinder cell metaplasia and low grade intraepithelial neoplasia in Barrett esophagus has previously been overestimated. The histological detection of dysplasia still remains the best biomarker for estimation of the risk of cancer of Barrett esophagus. Exact determination of invasion depth in the mucosa, respective submucosa is now established as prognostic marker for overall survival in Patients with early carcinomas and this classification is useful for therapy decisions (endoscopic versus surgical removal). In advanced Barrett carcinoma following neoadjuvant therapy the lymph node status (ypN) is a better prognostic factor than the ypT category. In metastasized tumors therapies targeting HER2/new, EGFR or c-Met have been investigated explicitly in Barrett carcinoma only in phase I/II studies, whereby the predictive value of appropriate molecular pathology investigations is not yet reliably established.

Long-Term Follow-up of Barrett’s Epithelium: Medical Versus Antireflux Surgical Therapy

BackgroundBarrett’s esophagus (BE) is the most serious complication of GERD. In BE patients, this observational study compares the effects of antireflux surgery versus antisecretory medical therapy. MethodsOverall, 89 BE patients (long BE = 45; short BE = 44) were considered: 45 patients underwent antireflux surgery and 44 underwent medical therapy. At both initial and follow-up endoscopy, symptoms were assessed using a detailed questionnaire; BE phenotypic changes [intestinal metaplasia (IM) presence/type, Cdx2 expression] were assessed by histology (H&E), histochemistry (HID), and immunohistochemistry. Surgical failures were defined as follows: (1) abnormal 24-h pH monitoring results after surgery, (2) endoscopically evident recurrent esophagitis, and (3) recurrent hiatal hernia or slipped fundoplication on endoscopy or barium swallow. ResultsReversion of IM was observed in 12/44 SSBE and 0/45 LSBE patients (p < 0.01). Reversion was more frequently observed after effective antireflux surgery than after medical treatment (p = 0.04). In patients with no further evidence of IM after therapy, Cdx2 expression was also absent (p = 0.02). The extent of IM was reduced, and the IM phenotype improved in SSBE patients after surgery. ConclusionsPatients with short BE (but not those with long BE) may benefit from surgically reducing the esophagus’ exposure to GE reflux; among these patients, successful surgery carries a higher IM reversion rate than medical treatment.

Role of brush cytology in the diagnosis of Barrett's esophagus: An analysis of eight cases

Although debatable, role of cytology in diagnosing Barrett's esophagus has been stressed by some authors. Our brief report analyses the role of brush cytology (BC) in its diagnosis. Eight patients who presented with upper gastrointestinal (GI) manifestations and subsequently diagnosed to have Barrett's esophagus with or without adenocarcinoma on brush cytology (BC) or, endoscopic biopsy (EB) or, a combination of both the techniques were included in the study. In all the cases routine cytologic smears and histologic sections with relevant special stains (when essential) were studied. On cytology, the diagnosis of "Barrett's esophagus" was made when the esophageal brushings obtained from a region beyond 3 cm from the gastroesophageal junction showed closely intermingled clusters of squamous and columnar cells, or when there was evidence of intestinal metaplasia. Adenocarcinoma in Barrett's esophagus was diagnosed by the usual criteria for malignancy with features of adenocarcinoma. Cytologic diagnoses were correlated with the histologic diagnoses. Of the eight cases, seven had histopathologic correlation of which six had evidence of BE on BC; four had cytohistologic concordance, of which three cases revealed adenocarcinoma arising in BE. Two endoscopic biopsies were nonrepresentative. In one case, cytology missed Barrett's esophagus. For two cases in which cytology detected Barrett's mucosa, biopsies were nonrepresentative. Our study showed brush cytology (BC) to be a fairly reliable test for detecting Barrett's esophagus. Owing to its inherent advantage of sampling a wider and circumferential area, a technically well performed brushing procedure is likely to be more representative and superior than multiple endoscopic biopsies.

The clinical value of narrow band imaging endoscopy in diagnosing intestinal metaplasla

Objective To investigate the morphologic features of gastric intestinal metaplasia (IM)using narrow band imaging(NBI)endoscopy,and its feasibility and accuracy for diagnosis of IM combined with histopathology.Methods The endoscopic examination was performed on 80 patients and suspected lesions associated with IM was further observed by NBI combined with magnifying endoscopy.The biopsy specimens were obtained from regions containing light blue crest(LBC)or non-LBC mucosa for pathological examination,and the results were analyzed.Results In 80 patients examined with NBI,IM was pathologically confirmed in 65 patients.Of which LBC was seen in 61 patients with a sensitivity of 94%and a specificity of 95%.In a total of 94 specimens obtained from LBC region,86 had histological evidence of IM with a positive predictive value of 9 1.49%.There was no evidence of IM in 79 out of 94 specimens obtained from non-LBC region of patients with or without LBC with a negative predictive value of 84.04%.The results indicated that the detective rate of IM could be increased if biopsy specimen was obtained from LBC region with help of NBI endoscopy(P＜0.05).Conclusions It has been demonstrated that NBI combined with magnifying endoscopy may improve the diagnosis of IM by clearly observing microvasculature and targeted-biopsy in LBC region,which is helpful in early diagnosis of gastric cancer. Key words: Gastric mucosa; Metaplasia; Intestinal mucosa; Endoscopic examination

Endoscopic Therapy for Barrett's Esophagus

Recent retrospective cohort data and a prospective randomized sham controlled trial have clearly documented the impact of endoscopic ablation therapy on dysplasia and Barrett's esophagus (BE). The clinical indications for ablation of BE includes high-grade dysplasia and intramucosal adenocarcinoma. The techniques of resection of mucosal irregularities and of ablation are reviewed, primarily thermal and photodynamic ablation. Ablation of BE with neoplasia has appropriately entered the clinical arena.

A Case Report of Pernicious Anemia and Recurrent Aphthous Stomatitis

The aim of this report is to present the management of a patient with pernicious anemia afflicted with recurrent aphthous stomatitis (RAS). RAS is one of the most common lesions of the oral mucosa. Although the exact etiology of RAS is still unknown different hematinic deficiencies have been proposed. Painful recurrent ulcers covered with a grayish pseudomembrane surrounded by an erythematous margin were identified on the tongue and in the buccal mucosa of a 71-year-old woman. The patient also presented with depapilation of the tongue. The clinical diagnosis was RAS. Laboratory tests including a hemogram were ordered to determine existing levels of folic acid, iron, ferritin, and vitamins B2, B6, and B12. Levels of serum vitamin B12 and serum hemoglobin were low. The laboratory investigation also showed a medium corpuscular volume of 104.1 fl. A gastroduodenoscopy revealed no macroscopic abnormality. A gastric biopsy showed mucosal atrophy in the gastric corpus with evidence of intestinal metaplasia. Antibodies against an intrinsic factor were negative. The diagnosis pernicious anemia was made, with RAS caused by vitamin B12 malabsorption. Treatment consisted of the administration of 1.0 ml of hydroxocolabamin intramuscularly twice weekly over four weeks followed by 1.0 ml once weekly for four weeks. Clinical resolution was observed after two months. The association of RAS with vitamin B12 malabsorption is a rare event. However, along with conventional RAS clinical management, iron, folic acid, vitamin B deficiencies, and nutritional intolerance must be considered. Evaluation of the predisposing factors is imperative in treating patients with RAS including vitamin B12 malabsorption. Determination of the levels of vitamin B12 should be the basis for replacement therapy. Such therapy can be considered a benefit to the patients with RAS as its etiology remains unclear. Clinicians must be alert to the possibility this lesion could be a signal of systemic disease.

Esophageal Adenocarcinoma

Esophageal Adenocarcinoma

Barrett’s Esophagus: a Discrepancy between Macroscopic and Histological Diagnosis

The diagnosis of Barrett's esophagus at present requires endoscopic and histological confirmation of specialized intestinal metaplasia. This study prospectively analyzed the endoscopic and histological prevalence of Barrett's esophagus and the risk factors for the presence of Barrett's esophagus among patients being treated in an endoscopy unit. A total of 474 unselected patients (58% men; mean age 52 y) were included in the study. Two biopsy specimens each were taken from below and above the squamocolumnar junction and from the antrum and gastric body. Four-quadrant biopsies were taken every 1-2 cm to confirm a macroscopic suspicion of Barrett's esophagus. Barrett's esophagus was suspected at endoscopy in 109 patients (23%). Of the 109 patients with endoscopically suspected Barrett's esophagus, only 46 (42%) had the finding confirmed histologically. The sensitivity and specificity for the endoscopic diagnosis of Barrett's esophagus were 62% and 84%, respectively. A multivariate logistic regression analysis identified age (P = 0.0001; odds ratio per life-year 1.087; 95% CI, 1.046-1.139), male sex (P = 0.0020; OR 6.346; 95% CI, 2.094-22.314), and the number of biopsies (P = 0.0025; OR 1.661; 95% CI, 1.247-2.392) as factors associated with evidence of intestinal metaplasia on biopsy. The striking discrepancy between the endoscopic findings and the histological diagnosis may be due to the focal distribution of intestinal metaplasia. This emphasizes the importance of an adequate biopsy protocol. In addition, better methods of detecting focal islands of intestinal metaplasia that are not visible at conventional endoscopy are needed.