Distribution of dysplasias and early invasive carcinoma in Barrett's esophagus

doi:10.1016/0046-8177(92)90123-K

Human Pathology

Volume 23, Issue 5, May 1992, Pages 479-482

https://doi.org/10.1016/0046-8177(92)90123-K Get rights and content

Abstract

To assess the anatomic relationships between areas of dysplasia and “early” carcinoma, we evaluated histologically the entire mucosal surfaces of seven esophagectomy specimens resected for high-grade dysplasia or early invasive (intramucosal and submucosal) carcinoma. We developed surface area maps and assessed the various degrees of dysplasia or carcinoma at 10 equidistant points. Our analysis shows an equal likelihood of high-grade dysplasia and/or early invasive carcinoma occurring throughout the length of Barrett's epithelium. Foci of carcinoma appear within fields of Barrett's epithelium and adjacent to areas of dysplasia, supporting a dysplasia-carcinoma sequence. The amount of dysplastic epithelium appears related to the surface area of Barrett's epithelium present. However, we found no association between the extent of dysplasia and the likelihood of finding carcinoma. This study supports the current standard of practice for clinical surveillance of patients with Barrett's esophagus by uniformly distributed endoscopic biopsy of the complete length. In addition, the presence of any degree of dysplasia may be an indication for close clinical follow-up.

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Management of Barrett's high-grade dysplasia: Initial results from a population-based national audit
2016, Gastrointestinal Endoscopy
Citation Excerpt :
The diagnosis of HGD is difficult. Dysplastic changes may be focal within a segment of BE, and early neoplastic changes are microscopic.23,24 This study found that in 40.0% of cases of HGD the mucosa was flat, and in 52.8% the lesion was unifocal.
Previous studies reported significant variation in the management of patients with Barrett’s esophagus. However, these are based on self-reported clinical practice. The aim of this study was to examine the management of high-grade dysplasia in Barrett’s esophagus in England by using patient-level data and to compare practice with guidelines.
From April 2012 to March 2013, National Health Service (NHS) trusts in England prospectively collected data on patients newly diagnosed with high-grade dysplasia (HGD) of the esophagus as part of the National Oesophago-Gastric Cancer Audit. Data were collected on patient characteristics, diagnosis and endoscopic findings, treatment planning, and therapy.
Between April 2012 and March 2013, NHS trusts reported 465 cases of HGD. Diagnosis was confirmed by a second pathologist in 79.4% of cases (270/340), and 86.0% (374/465) had their treatment planned at a multidisciplinary team meeting. A total of 290 patients (62.4%) were managed endoscopically (frequently with endoscopic resection or radiofrequency ablation), whereas 26 patients (5.6%) had esophagectomy. The proportion of patients managed by surveillance varied by age (P < .001), ranging from 19.5% in patients aged <65 years to 63.8% in patients aged ≥85 years. More patients received active treatment if their cases were discussed at a multidisciplinary meeting (73.5% vs 44.3%; P < .001) or managed at higher-volume trusts (87.8% vs 55.4%; P < .001).
There was marked variation in the management of HGD across England, with a third of patients receiving no active treatment. Patients discussed at a specialist multidisciplinary meeting or managed in high-volume trusts were more likely to receive active treatment.
Diagnosis and Surveillance of Barrett's Esophagus
2011, Clinical Gastrointestinal Endoscopy, Second Edition
Adherence to Biopsy Guidelines for Barrett's Esophagus Surveillance in the Community Setting in the United States
2009, Clinical Gastroenterology and Hepatology
Current surveillance guidelines for Barrett's esophagus (BE) recommend extensive biopsies to minimize sampling error. Biopsy practice patterns for BE surveillance in the community have not been well-described. We used a national community-based pathology database to analyze adherence to guidelines and to determine whether adherence was associated with dysplasia detection.
We identified 10,958 cases of established BE in the Caris Diagnostics pathology database from January 2002–April 2007. Demographic, pathologic, and endoscopic data were recorded. Dysplasia was categorized as low grade, high grade, or adenocarcinoma. Adherence was defined as ≥4 esophageal biopsies per 2 cm BE or a ratio ≥2.0. Generalized estimating equation multivariable analysis was performed to assess factors associated with adherence, adjusted for clustering by individual gastroenterologist.
A total of 2245 BE surveillance cases were identified with linked endoscopy reports that recorded BE length and could be assessed for adherence. Adherence to guidelines was seen in 51.2% of cases. In multivariable analysis, longer segment BE was associated with significantly reduced adherence (3–5 cm, odds ratio [OR] 0.14, 95% confidence interval [CI] 0.10–0.19; 6–8 cm, OR 0.06, 95% CI 0.03–0.09; ≥9 cm, OR 0.03, 95% CI 0.01–0.07). Stratified by BE length, nonadherence was associated with significantly decreased dysplasia detection (summary OR 0.53, 95% CI 0.35–0.82).
Adherence to BE biopsy guidelines in the community is low, and nonadherence is associated with significantly decreased dysplasia detection. Future studies should identify factors underlying nonadherence as well as mechanisms to increase adherence to guidelines to improve early detection of dysplasia.
Risk Factors for Esophageal Cancer Development
2009, Surgical Oncology Clinics of North America
Molecular Mechanisms of Cholangiocarcinogenesis: Are Biliary Intraepithelial Neoplasia and Intraductal Papillary Neoplasms of the Bile Duct Precursors to Cholangiocarcinoma?
2009, Surgical Oncology Clinics of North America
Cholangiocarcinoma (CC) is a rare, malignant neoplasm that can develop from any site within the intrahepatic or extrahepatic biliary tree. Although the key steps of cholangiocarcinogenesis remain unknown, it has been hypothesized that CC may develop through two key premalignant precursor lesions: biliary intraepithelial neoplasia (BilIN) and intraductal papillary neoplasm of the bile duct (IPNB). These lesions probably are analogous to pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasm, respectively. This article outlines the molecular basis of cholangiocarcinogenesis through the BilIN and IPNB pathways. It highlights the genetic mutations that alter cellular proliferation, tumor suppression, and impairment of critical mucinous, cell-adhesion, and matrix proteins.
Cancer after repair of esophageal atresia: population-based long-term follow-up
2008, Journal of Pediatric Surgery
Esophageal atresia (EA) predisposes to gastroesophageal reflux that is associated with intestinal metaplasia and may result in development of adenocarcinoma of the esophagus. To date, the literature has reported 5 cases of esophageal cancer in adult patients treated for EA. The aim of this study was to find out the incidence of esophageal cancer in adult patients with repaired EA.
Five hundred two consecutive patients treated for EA from 1949 to 1978 were followed-up for cancer through the files of the population-based countrywide cancer registry from 1967 to 2004. The number of cancer cases observed and person-years at risk were counted, and the expected number of cancer cases estimated from the national cancer incidence rates. The standardized incidence ratios (SIRs) were calculated by dividing the number of cancer cases observed by the expected numbers.
None of the 502 patients were lost to follow-up; 230 patients who died before 1967 younger than the median age of 8 days were excluded from further analysis. The 272 remaining patients (142 males) were eligible for follow-up (median age, 35 years; range, 2 days to 56 years). Three cases of cancer were found (SIR, 1.0; 95% confidence interval, 0.20-2.8). One was lymphoma in small intestine, 1 was leukemia, and 1 carcinoma of the uterus but no cases of esophageal cancer.
Our study is able to exclude long-term risk for esophageal cancer after repair of EA 500-fold higher than that of the normal population. Considering the relatively young age of the survivors, further studies and continued follow-up are warranted to elucidate risk for esophageal cancer and need for endoscopic surveillance after repair of EA.

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Original contributionDistribution of dysplasias and early invasive carcinoma in Barrett's esophagus

Abstract

Gastroenterology

Gastroenterology

Barrett's esophagus

N Engl J Med

The incidence of adenocarcinoma in columnar-lined (Barrett's) esophagus

N Engl J Med

Barrett's esophagus, correlation between mucin histochemistry, flow cytometry and histologic diagnosis for predicting increased cancer risk

Am J Pathol

Original contribution
Distribution of dysplasias and early invasive carcinoma in Barrett's esophagus