Controversies in the Diagnosis of Barrett Esophagus and Barrett-Related Dysplasia: One Pathologist's Perspective

2010 ◽  
Vol 134 (10) ◽  
pp. 1479-1484 ◽  
Author(s):  
John R. Goldblum

Abstract Context.—Pathologists frequently assess esophageal biopsy specimens to “rule out Barrett esophagus,” as well as to assess for the presence or absence of dysplasia. Objective.—To review some of the recent controversies in the diagnosis of Barrett esophagus and Barrett-related dysplasia. Data Sources.—Sources were the author's experience and review of the English literature from 1978 to 2009. Conclusions.—Although goblet cells are required by the American College of Gastroenterology to confirm a diagnosis of Barrett esophagus, this definition might expand to include columnar-lined esophagus without goblet cells. The recognition of dysplasia in Barrett esophagus remains a difficult task for the surgical pathologist, with difficulties in distinguishing reactive epithelium from dysplasia, low-grade dysplasia from high-grade dysplasia, and even high-grade dysplasia from intramucosal adenocarcinoma.

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 117-118
Author(s):  
D Maillet ◽  
E Desilets ◽  
T Maniere

Abstract Background Endoscopic submucosal dissection (ESD) is an endoscopic procedure developed in Asian countries to treat early gastric cancer (EGC). Western countries have less experience with this challenging technique. Aims The goal of this study is to evaluate the effectiveness of ESD as a preliminary experience. Methods This is an unicentric retrospective study of all consecutive gastric ESD for adenomas or EGC from 07/2017 to 08/2020. The primary endpoints were en bloc and R0 resection rates. Results Nineteen patients (mean age 74.2 (54–88), sex ratio 3F/16M) and 23 lesions were included. Mean diameter was 25 mm (10–90). Treatment was previously performed in 7 cases (30.4%), by ESD (5) or EMR (2). The procedure, performed under general anaesthesia, lasted on average 148 minutes (45–412). En bloc resections were performed in 16 cases (69.6%); 5 cases (21.7%) were converted to P-EMR and there was a failure to resect the lesion because of deep invasion or perforation in 2 cases (8.7%). Pathologic examination demonstrated 2 low-grade dysplasia, 4 high-grade dysplasia and 15 adenocarcinomas: intramucosal (8), sm1 (2), sm2 (2), sm3 (1) or sm deep (2). R0 and curative resection rates were 43.5% and 39.1% respectively. The complication rate related to the procedure was 30.4% including 5 perforations and 2 delayed bleeding: all were managed endoscopically. Five patients (21.7%) underwent subsequent gastrectomy for non-curative resection (4) or failed resection (1); 3 had no residual disease on final pathology, 1 had high grade dysplasia and 1 had intramucosal adenocarcinoma. One patient went to palliative care because he was unfit for surgery. Follow-up endoscopy was completed in all 17 patients who underwent endoscopic resection (mean 10 months (2–24)). Recurrence occurred in 23.5% (4/17); all were successfully treated by another ESD. Conclusions In our preliminary experience, the rate of en bloc and R0 resection were 70% and 44%. Compared to other studies, these low en bloc and curative resection rates may be explained by technically difficult lesions during the learning curve and might improve with experience. Nevertheless, surgery has been avoided in 13/19 patients (68%) with endoscopic intervention. Funding Agencies None


2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 20-20 ◽  
Author(s):  
Allon Kahn ◽  
Vishnu Kommineni ◽  
Jonathan Callaway ◽  
Rahul Pannala ◽  
David Fleischer ◽  
...  

20 Background: Esophageal adenocarcinoma (EAC) incidence is rising and prognosis is uniformly poor, even with early stage disease. Barrett esophagus (BE) serves as a premalignant marker for EAC, with an estimated progression of 0.5% per year. Low-grade (LGD) and high-grade dysplasia (HGD) confer a higher risk of progression, providing an opportunity for intervention and surveillance. Aims: To evaluate a large cohort of patients undergoing endoscopic evaluation of BE and thereby better understand the natural history of BE and dysplasia. Methods: A retrospective review of endoscopic databases was conducted for all patients with the diagnosis of BE undergoing upper endoscopy at a tertiary academic medical center from 1991-2010. All endoscopy and accompanying pathology reports were reviewed. Only those patients with 2 biopsies documenting specialized intestinal metaplasia were analyzed. Results: 848 patients underwent upper endoscopy for evaluation of BE. Of these, 674 patients met inclusion criteria, at a mean follow up of 66.6 months. Table 1 depicts the distribution of patients according to their histology at presentation. 22 (3.2%) patients presented with established EAC, while EAC developed in 51 (7.6%). Of patients with HGD, LGD, or no dysplasia (ND) at presentation, EAC ultimately developed in 30.6%, 6.6%, and 2.7%, respectively. EAC developed in 4 patients despite RFA treatment for ND (2) or LGD (2). HGD developed in 6 such patients after treatment for ND (3) and LGD (3). Only 1 patient in each RFA-treated cohort required esophagectomy, while the others cleared dysplasia or EAC with continuous treatment. Conclusions: In this large cohort of patients with Barrett’s esophagus, higher grade of dysplasia at first endoscopy was associated with development of EAC. Continuous surveillance during and after endoscopic treatment is necessary and often results in clearance of dysplasia and EAC. [Table: see text]


2008 ◽  
Vol 132 (10) ◽  
pp. 1577-1585 ◽  
Author(s):  
Robert D. Odze

Abstract Context.—At present, Barrett esophagus is the most common cause of esophageal adenocarcinoma. In the past 20 years, the incidence of esophageal adenocarcinoma in white males has exceeded that of tumors of the colorectum, lung, prostate, and skin. Objectives.—To (1) provide an evidence-based review of the diagnosis, classification, and histologic differentiation of Barrett esophagus from gastric carditis, (2) provide a summary of the key pathologic features of precursor lesions, such as dysplasia, and (3) evaluate adjunctive markers of dysplasia and predictive markers for the development of cancer. The natural history and risk of cancer in patients with Barrett esophagus is also reviewed. Data Sources.—For this review, selected published peer reviewed articles were chosen from a search through PubMed between the years 1970 and 2007. Conclusions.—The current definition of Barrett esophagus is partially flawed because not all cases are endoscopically recognizable, nongoblet epithelium is biologically intestinalized, and determination of the presence or absence of goblet cells is susceptible to sampling error. Differentiation of ultrashort segment Barrett esophagus from chronic gastric carditis can be accomplished, in a minority of cases, by evaluating for the presence or absence of histologic features that are known to be associated with Barrett esophagus. Dysplasia in Barrett esophagus begins in the crypt bases and then extends more superficially to include the upper portions of the crypts and surface epithelium. Low- and high-grade dysplasia are distinguished by the presence of marked cytologic and/or architectural abnormalities in the latter compared with the former. There are few, if any, reliable adjunctive diagnostic techniques that can help differentiate nondysplastic from dysplastic epithelium. However, α-methylacyl coenzyme A racemase staining has been shown to be useful in 2 separate studies. Both low- and high-grade dysplasia are progressive lesions, and in general, the extent of dysplasia, particularly low grade, is a strong risk factor for progression to carcinoma. Of all the biologic and genetic biomarkers studied to date, evaluation of DNA content is the most reliable and specific. The management of patients with dysplasia is variable among institutions and ranges from aggressive surveillance, endoscopic mucosal resection, mucosal ablation, or total esophagectomy.


2014 ◽  
Vol 23 (2) ◽  
pp. 161-170 ◽  
Author(s):  
Claudiu Margaritescu ◽  
Daniel Pirici ◽  
Irina Cherciu ◽  
Alexandru Barbalan ◽  
Tatiana Cârtâna ◽  
...  

Background & Aims: Colorectal cancer represents the third most common malignancy and the fourth most common cause of cancer death worldwide. The existence of drug-resistant colon cancer stem cells is thought to be one of the most important reasons behind treatment failure in colon cancer, their existence putatively leading to metastasis and recurrences. The aim of our study was to investigate the immunoexpression patterns of CD133 and CD166 in colon carcinoma, both individually and in combination, assessing their significance as prognostic markers.Methods. A total of 45 retrospective colon adenocarcinoma cases were investigated by enzymatic and multiple fluorescence immunohistochemistry for their CD133 and CD166 expression and colocalization.Results. Both CD133 and CD166 were expressed to different extents in all cancer specimens, with apredominant cytoplasmic pattern for CD133 and a more obvious membranous-like pattern for CD166.Overall, when comparing their reactivity for the tumoral tissue, CD166 expression areas seemed to be smaller than those of CD133. However, there was a direct correlation between CD133 and CD166 expression levels throughout the entire spectrum of lesions, with higher values for dysplastic lesions. Colocalization of CD133/ CD166 was obvious at the level of cells membranes, with higher coeficients in high grade dysplasia, followed by well and moderate differentiated tumours.Conclusions. CD133/CD166 colocalization is an early event occurring in colon tumorigenesis, with thehighest coeficients recorded for patients with high grade dysplasia, followed by well differentiated tumours. Thus, we consider that the coexpression of these two markers could be useful for further prognostic andtherapeutically stratification of patients with colon cancer.Abbreviations: AJCC - American Joint Committee on Cancer; CCD - charge-coupled device camera sensor; CD133 - prominin-1 (PROM1); CD166 - Activated Leukocyte Cell Adhesion Molecule (ALCAM); CRC - colorectal cancer; CSC - cancer stem cells; DAB - 3,3'-diaminobenzidine chromogen; DAPI - 4',6-diamidino- 2-phenylindole; HE - Hematoxylin and eosin staining; HGD - high grade dysplasia; HRP - horseradish peroxidase; LGD - low grade dysplasia; SDS - sodium dodecyl sulfate*Part of this work has been accepted as a poster presentation at the Digestive Disease Week (DDW) meeting, Chicago, IL, USA May 3-6, 2014


2007 ◽  
Vol 65 (5) ◽  
pp. AB151 ◽  
Author(s):  
Joep J. Gondrie ◽  
Roos E. Pouw ◽  
Carine Sondermeijer ◽  
Wilda D. Rosmolen ◽  
Femke Peters ◽  
...  

2003 ◽  
Vol 48 (2) ◽  
pp. 43-45 ◽  
Author(s):  
E F Shen ◽  
S Gladstone ◽  
G Milne ◽  
S Paterson-Brown ◽  
I D Penman

Management of columnar lined oesophagus (CLO; Barrett s oesophagus) is controversial. We prospectively audited surveillance practices in Scotland and prospectively assessed the impact of introducing local guidelines for Barrett s surveillance in Edinburgh. Most respondents were gastroenterologists. The majority take random, not four quadrant, biopsies from the CLO. In Edinburgh during 2000, 80 patients underwent surveillance. The guideline protocol was not followed in 30 (37.5%) patients. Follow up of patients without dysplasia generally conformed to the guidelines. Follow up of patients with low grade dysplasia was highly variable while management of those with high grade dysplasia followed the guidelines. Overall we found a wide variability in the management and surveillance of CLO. Early experience suggests that implementation of guidelines is helpful but there is still variation in practice.


Author(s):  
K Y Song ◽  
A J Henn ◽  
A A Gravely ◽  
H Mesa ◽  
S Sultan ◽  
...  

SUMMARY Patients with Barrett's esophagus (BE) and low-grade dysplasia (LGD) are at increased risk of esophageal adenocarcinoma (EAC), although many regress to nondysplastic BE. This has significant clinical importance for patients being considered for endoscopic eradication therapy. Our aim is to determine the risk for progression in patients with confirmed persistent LGD. We performed a single-center retrospective cohort study of patients with BE and confirmed LGD between 2006 and 2016. Confirmed LGD was defined as LGD diagnosed by consensus conference with an expert GI pathologist or review by an expert GI pathologist and persistence as LGD present on subsequent endoscopic biopsy. The primary outcome was the incidence rate of HGD (high-grade dysplasia)/EAC. Secondary outcomes included risk factors for dysplastic progression. Risk factors for progression were assessed using univariate and multivariate analysis with logistic regression. Of 69 patients (mean age 65.2 years) with confirmed LGD were included. In total, 16 of 69 patients (23.2%) with LGD developed HGD/EAC during a median follow-up of 3.74 years (IQR, 1.24–5.45). For persistent confirmed LGD, the rate was 6.44 (95% confidence interval (CI), 2.61–13.40) compared to 2.61 cases per 100 patient-years (95% CI, 0.83–6.30) for nonpersistent LGD. Persistent LGD was found in only 29% of patients. Persistent LGD was an independent risk factor for the development of HGD/EAC (OR 4.18; [95% CI, 1.03–17.1]). Persistent confirmed LGD, present in only 1/3 of patients, was an independent risk factor for the development of HGD/EAC. Persistence LGD may be useful in decision making regarding the management of BE.


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