Adenocarcinoma of the lower esophagus with Barrett's esophagus or without Barrett's esophagus: differences in patients' survival after preoperative chemoradiation

It remains unclear whether the overall survival (OS) of patients with localized esophageal adenocarcinoma (LEA) with Barrett's esophagus (BE) (Barrett's-positive) and those with LEA without BE (Barrett's-negative) following preoperative chemoradiation is different. Based on the published differences in the molecular biology of the two entities, we hypothesized that the two groups will have a different clinical biology (and OS). In this retrospective analysis, all patients with LEA had surgery following preoperative chemoradiation. Apart from age, gender, baseline clinical stage, location, class of cytotoxics, post-therapy stage, and OS, LEAs were divided up into Barrett's-positive and Barrett's-negative groups based on histologic documentation of BE. The Kaplan-Meier and Cox regression analytic methods were used. We analyzed 362 patients with LEA (137 Barrett's-positive and 225 Barrett's-negative). A higher proportion of Barrett's-positive patients had _EUST2 cancers (27%) than those with Barrett's-negative cancer (17%). More Barrett's-negative LEAs involved gastroesophageal junction than Barrett's-positive ones ( P  = 0.001). The OS was significantly shorter for Barrett's-positive patients than that for Barrett's-negative patients (32 months vs. 51 months; P  = 0.04). In a multivariate analysis for OS, Barrett's-positive LEA ( P  = 0.006), old age ( P  = 0.016), baseline positive nodes ( P  = 0.005), more than 2 positive _ypN ( P  = 0.0001), higher _ypT ( P  = 0.003), and the use of a taxane (0.04) were the independent prognosticators. Our data demonstrate that the clinical biology (reflected in OS) is less favorable for patients with Barrett's-positive LEA than for patients with Barrett's-negative LEA. Our intriguing findings need confirmation followed by in-depth molecular study to explain these differences.     

Adenocarcinoma arising in Barrett's esophagus

The main goal of this study was to evaluate the development of adenocarcinoma in patients with Barrett's esophagus. During the period from January 1975 to December 1985, a total of 134 patients had endoscopically severe esophagitis and/or Barrett's esophagus. In these patients, 32 (24%) met the macroscopic and histologic criteria for the diagnosis of Barrett's esophagus. A check-up study of these patients was performed in 1987. Adenocarcinoma developed in three patients during the follow-up period of 166.1 patient-years. Dysplasia in the columnar epithelium was found in two of these patients six and 15 months before the diagnosis of adenocarcinoma. The third patient with adenocarcinoma was detected in endoscopic follow-up in 1987. In addition, the endoscopic examination showed unchanged Barrett's epithelium in all but three patients despite the operative and/or medical treatment 3–12 years (mean 6.7 years) earlier. We conclude that Barrett's esophagus is a potential premalignant condition and careful endoscopic surveillance for dysplasia in the columnar epithelium of the distal esophagus is mandatory in patients with Barrett's esophagus.     

Adenocarcinoma and Barrett's esophagus. An overrated risk?

The risk of developing esophageal cancer in Barrett's esophagus has been estimated at about 10%. This estimate is based primarily on data concerning the prevalence of that association in series of hospitalized patients and autopsies--a practice that tends to exaggerate the risk. We have reviewed retrospectively our experience with 115 patients whom we treated for Barrett's esophagus between September 1962 and March 1983, and have distinguished our data on the prevalence of esophageal cancer from that on incidence. For 8 patients, we found both Barrett's esophagus and esophageal adenocarcinoma during the initial evaluations for a prevalence ratio of 7%. We followed 105 patients not found to have esophageal cancer initially for a total of 350 person-years. Only 2 patients developed adenocarcinoma during that follow-up period for an incidence of 1 case per 175 person-years. This incidence, although some 40-fold greater than that of the general population, is substantially lower than previously estimated. Routine endoscopic and histologic surveillance has been recommended for patients with Barrett's esophagus because of the alleged high incidence of esophageal cancer. Inasmuch as that incidence now appears to be low, we question the value of such surveillance for these patients.     

Adenocarcinoma arising in Barrett's esophagus after total gastrectomy

A 64-yr-old Japanese male who underwent a partial gastrectomy for a duodenal ulcer at the age of 21, a total resection of the remnant stomach for a stomal ulcer at age 25, and in whom Barrett's esophagus was diagnosed at age 47, was found to have a tumor at the distal esophagus and was operated on by thoracic esophagectomy. The tumor was a well to moderately differentiated adenocarcinoma invading down to the muscularis propria. The entire esophageal mucosa in the resected specimen was lined by columnar epithelium. This tumor was thought to derive from the Barrett's esophageal epithelium.     

Adenocarcinoma complicating Barrett's esophagus: an analysis of cell proliferation

Received: May 9, 2000 / Accepted: July 28, 2000     

Barrett's esophagus. A prevalent, occult complication of gastroesophageal reflux disease

A prospective study of patients with symptoms of gastroesophageal reflux was undertaken to determine the prevalence of Barrett's esophagus and reevaluate the diagnostic approach necessary to detect this complication. Endoscopy with mucosal biopsy was performed in 97 subjects. Twelve (12.4%) were found to have Barrett's esophagus. The sensitivity and specificity of the endoscopic and radiologic examinations for Barrett's esophagus were prospectively evaluated. Endoscopy (92%) was significantly more sensitive than radiology (24%) in detecting Barrett's esophagus (p less than 0.001). The frequency and severity of reflux symptoms among patients determined to have Barrett's esophagus, reflux esophagitis, or normal esophageal biopsies were quantitatively similar in all three groups, except for significantly greater daytime heartburn in those with reflux esophagitis (p less than 0.01). These data indicate that Barrett's esophagus complicates gastroesophageal reflux more often than previously believed.     

Barrett's esophagus and medications that relax the lower esophageal sphincter

OBJECTIVES: Medications that may increase gastroesophageal reflux could be risk factors for esophageal adenocarcinoma; however, epidemiologic studies present conflicting results. We evaluated patients with a high-risk condition, Barrett's esophagus, to identify risk factors that may act early in the carcinogenic process. METHODS: We conducted a nested case-control study within a large integrated health-services organization. Electronic databases were used to identify incident diagnoses of Barrett's esophagus (cases); two controls were matched to each case. Electronic databases provided information on the use of medications that may induce reflux (nitrates, calcium channel blockers, xanthines, benzodiazepines, and beta agonists) and potential confounders. A supplemental mailed questionnaire evaluated additional potential confounders. RESULTS: We identified 421 cases and selected 842 controls. The association between any medication use and a Barrett's esophagus diagnosis was modified by age; an increased risk was observed only among subjects <70 yr of age (adjusted odds ratio [OR] = 2.6; 95% confidence interval [CI] 1.5-4.6). A Barrett's esophagus diagnosis was associated with asthma medication use (OR 5.8; 95% CI 2.2, 14.9), but not with the other medications studied. Subgroup analyses suggested that medication use was not independently associated with reflux symptoms and that adjustment for asthma symptoms substantially reduced the association between medication use and a Barrett's esophagus diagnosis. CONCLUSION: The use of medications that may induce reflux was associated with a Barrett's esophagus diagnosis among younger persons. This association was only observed with asthma medications; the analyses suggested the possibility of confounding by indication, whereby reflux may cause both asthma and Barrett's esophagus.     

Adenocarcinoma esophagus with choroid metastasis.

Metastases to the eye are rare and those from carcinoma esophagus are very rare, with only one report in the English literature. We report a 46-year-old man with adenocarcinoma of esophagus who developed isolated choroid metastasis after definitive treatment of the primary tumor.     

Tongue-like Barrett＇s esophagus is associated with gastroesophageal reflux disease

AIM： To test this hypothesis of barrett esophagus （BE） classified into two types and to further determine if there was any correlation between the shape of endoscopically suspected esophageal metaplasia （ESEM）, prevalence of reflux esophagitis （RE） and heartburn. METHODS： A total of 6504 Japanese who underwent endoscopy for their annual stomach check-up were enrolled in this study. BE was detected without histological confirmation that is ESEM. We originally classified cases of ESEM into 3 types based on its shape： Tongue-like （T type）, Dome-like （D type） and Wave-like （W type） ESEM. The respective subjects were prospectively asked to complete questionnaires concerning the symptoms of heartburn, dysphagia, and abdominal pain for a one-month period. RESULTS： ESEM was observed in 10.3% of 6504 subjects （ESEM 〈 1 cm, 9.4%; 1cm≤ESEM 〈 3 cm, 1.7%; ESEM≥3 cm, 0.5%）. The frequency of ESEM was significantly higher in males compared with female subjects. Statistical analysis showed that the prevalence of heartburn and RE were significantly higher in the T type ESEM than in the W type ESEM （P 〈 0.05）. CONCLUSION： The T type ESEM was strongly associated with reflux symptoms and RE whereas the W type ESEM was not associated with GERD.     

Barrett's esophagus and achalasia. A case report.

A 70-year-old woman with no previous gastroesophageal surgery gave a 6-month history of dysphagia. Barium studies suggested a diagnosis of achalasia. Esophageal manometry showed absence of peristalsis and a high lower esophageal sphincter pressure. Endoscopy showed a dilated esophagus with food residue, and Barrett's esophagus was present. The association of Barrett's esophagus and achalasia must be rare.     

Gastrin content of columnar mucosa lining the lower (Barrett's) esophagus

Tissue gastrin was determined in 36 biopsies obtained from the esophagus and 35 biopsies from the stomach in 12 patients with Barrett's esophagus. Histology of the mucosa from the area adjacent to the biopsy sites was also examined. Esophageal biopsies were obtained from three different sites in each patient. The gastric biopsies were obtained from the antrum, fundus, and the area just distal to the lower border of the lower esophageal sphincter. The columnar mucosa lining the esophagus was of three distinct types, namely, fundic, transitional (cardiac), or specialized. None of these epithelia nor the squamous epithelium showed any detectable gastrin. In contrast, antral mucosa had very high gastrin content; smaller amounts of gastrin were detected in duodenal epithelium, whereas fundic mucosa sometimes contained small amounts of gastrin.Supported by Southwestern Medical Foundation, and by Research Grants AM 13711 and CA 15332 from the National Institutes of Health, and DT-17 from the American Cancer Society     

Mechanisms of disease: Carcinogenesis in Barrett's esophagus

The pathogenesis of cancer in Barrett's esophagus is multifactorial. Gastroesophageal reflux seems to be important in the initiation of Barrett's esophagus, but its role in promoting carcinogenesis has yet to be established. Diet, lifestyle and carcinogens, especially the nitrates, may be important in the development of carcinogenesis, and require further investigation. Inhibition of reflux-stimulated inflammatory changes, for example by inhibiting cyclooxygenase, holds promise for decreasing cancer progression. Similarly, dietary and lifestyle modification used in the management of reflux may also help to prevent the development of esophageal cancer. The molecular changes that are associated with the development of cancer in Barrett's esophagus offer several potential areas of intervention to prevent and manage esophageal cancer. Limiting cell growth, increasing apoptosis of damaged cells, limiting cell invasion and angiogenesis factors could be useful to accomplish this goal. Having a greater understanding of the pathogenesis of this condition can only help to develop more management options in the future.     

Health-related quality of life and severity of symptoms in patients with Barrett's esophagus and gastroesophageal reflux disease patients without Barrett's esophagus

OBJECTIVES: The aims of this study were: 1) to compare the health-related quality of life (HRQL) of patients with Barrett's esophagus (BE) to that of patients with GERD who did not have BE; 2) to compare HRQL of gastroesophageal reflux disease (GERD) patients to that of normative data for the US general population; and 3) to examine the impact of GERD symptom frequency and severity on HRQL. METHODS: The SF-36 and a validated GERD questionnaire were administered to 107 patients with biopsy-proven BE and to 104 patients with GERD but no BE by endoscopy. Frequent symptoms were defined as symptoms that occurred at least once weekly. Severity of symptoms was rated on a scale from 1 to 4 (mild to very severe). RESULTS: In all, 85% of the GERD patients and 82% of BE patients completed the questionnaires. There was no difference in the scores of the eight subscales of the SF-36 between BE patients and those with GERD but without BE (p > 0.05). However, both groups scored below average on all subscales of the SF-36 compared to published US norms for an age- and gender-matched group. Using multivariable linear regression, the social functioning subscale of the SF-36 correlated with the presence of heartburn or acid regurgitation, severity of acid regurgitation, frequency of heartburn, frequency of acid regurgitation, and number of comorbidities. Similarly, the physical functioning subscale correlated with age, frequency of heartburn, and number of comorbidities. The bodily pain subscale correlated with the frequency of heartburn and number of comorbidities. The bodily pain subscale correlated with the frequency of heartburn and the severity of dysphagia, whereas the role emotional subscale correlated with the frequency of heartburn and the presence of dysphagia. CONCLUSIONS: Although there were no differences in HRQL between BE and GERD patients, both groups scored below average on the subscales of the SF-36 compared to normal controls. GERD symptom frequency and severity were associated with bodily pain and with impaired social, emotional, and physical functioning, suggesting a profound impact on daily living.     

Barrett's esophagus. Update of the endoscopic treatment

Actual Barrett's esophagus management includes symptomatic approach for GERD in order to prevent erosive injury and endoscopic & histologycal surveillance to detect dysplasia and early cancer. In high-grade dysplasia and superficial carcinoma, less aggressive procedures has been attempted to avoid extended surgery, such as Argon Plasma Coagulator, Multipolar Coagulation, Heater Probe, Photodynamic Therapy, and recently radiofrequency local treatment, associated or not to antireflux surgery. Ultrasonic therapy and Cryotherapy are new approaches, which are under clinical investigation. Barrett's epithelium resection utilizing endoscopical mucosal resection is a new promising procedure, which comes to the arena, allowing besides the compromised epithelium removal, its complete pathological evaluation and probably a curative intent. The actual revision intents to discuss the results of the different alternatives at the platform of treatment in dysplastic Barrett's or early carcinoma growing in the Barrett's epithelium.     

Barrett's esophagus and esophageal adenocarcinoma.

Barrett's esophagus is a condition in which the normal stratified squamous epithelium is replaced by a specialized metaplastic columnar epithelium. It develops as a consequence of chronic gastroesophageal reflux and predisposes to the development of esophageal adenocarcinoma. Adenocarcinoma develops in Barrett's esophagus by a multistep process in which specialized metaplasia progresses to dysplasia, then to early adenocarcinoma, and eventually to deeply invasive and metastatic disease. This neoplastic progression is associated with a process of genomic instability that generates abnormal clones of cells, some of which have aneuploid or increased G2/tetraploid DNA content. A systematic protocol of endoscopic biopsy can detect Barrett's adenocarcinomas at an early stage, when they may be curable.