Barrett's esophagus in patients with symptomatic reflux esophagitis

We evaluated the frequency with which Barrett's esophagus (BE) occurs in patients with symptomatic reflux esophagitis, and compared the clinical endoscopic and manometric features of patients with Barrett's esophagus with those of patients who had non-Barrett's esophagitis (NBE). The effect of 6 months' medical treatment on BE patients was reevaluated by repeating manometry, endoscopy, and biopsy. Esophageal manometry was performed by perfusion technique and endoscopic biopsies were obtained. There were 180 patients; 20 (11%) were found to have BE. The vast majority of BE patients were caucasians. BE patients had symptoms of gastroesophageal reflux for a longer time than did NBE patients. Mean lower esophageal sphincter pressure in BE patients was lower than that in NBE patients. On medical treatment, the severity of esophagitis as judged by endoscopic criteria in BE patients was reduced, but there was no increase in lower esophageal sphincter pressure and no regression of the columnar epithelium.     

Identification of Barrett's esophagus in relatives by endoscopic screening

AIM: Familial aggregation of Barrett's esophagus and its associated cancers has been termed familial Barrett's esophagus (FBE). The aim of the study was to determine whether endoscopic screening would identify Barrett's esophagus (BE) in relatives of probands with BE or esophageal adenocarcinoma (EAC). METHODS: All living first-degree relatives of patients with long segment BE or EAC presenting to the endoscopy suite of two academic hospitals were sent validated questionnaires inquiring about gastroesophageal reflux symptoms and prior endoscopic evaluation. First-degree relatives of affected probands or affected relatives who reported no prior upper endoscopy were offered screening unsedated esophagoscopy. Relatives with chronic gastroesophageal reflux symptoms were also offered an alternative of conventional sedated upper endoscopy. The yield of screening endoscopy was measured. Screening endoscopy findings were then compared between family members of known FBE patients and those with "isolated" disease. RESULTS: One hundred and ninety-eight relatives from 69 families, 23 known FBE probands and 46 probands with apparently "isolated" disease, were enrolled. Forty relatives (29 FBE relatives and 11 relatives of probands with "isolated" disease) reported prior upper endoscopy. Screening upper endoscopies performed on 62 (25 FBE and 37 "isolated" disease relatives) of the remaining 158 relatives identified Barrett's epithelium in 13 (21%). Compared to probands with apparently "isolated" disease, Barrett's epithelium (EAC, BE, or SSBE) was identified significantly more often in siblings and offspring of FBE probands, p相似文献   

Barrett's esophagus in scleroderma: increased prevalence and radiographic findings

Ten of 27 patients (37%) with scleroderma who underwent endoscopy at our hospital between 1980 and 1984 for symptoms of reflux esophagitis had biopsy-proven Barrett's esophagus. Two of those 10 patients had esophageal adenocarcinomas. In a blinded review of esophagrams (all but 2 using double-contrast technique) from 16 of the 27 patients, only 1 patient was thought to be at high risk for Barrett's esophagus due to a high esophageal stricture with an adjacent reticular pattern of the mucosa. The latter patient had biopsy-proven Barrett's mucosa. Eight patients were thought to be at moderate risk for Barrett's esophagus due to reflux esophagitis and/or distal strictures in 6 and polypoid intraluminal masses in 2. Three of the 6 patients with esophagitis and/or strictures had Barrett's esophagus, and both patients with masses had adenocarcinomas arising in Barrett's mucosa. Finally, 7 patients who had no esophagitis or strictures were thought to be at low risk for Barrett's esophagus. None of those 7 had histologic evidence of Barrett's mucosa. Thus, the major value of double-contrast esophagography is its ability to classify patients into high-, moderate-, and low-risk for Barrett's esophagus to determine the relative need for endoscopy and biopsy in these patients.     

Barrett's esophagus: prevalence and size of hiatal hernia

OBJECTIVE: Barrett's esophagus is caused by gastroesophageal reflux and predisposes to adenocarcinoma. Hiatal hernia may cause reflux. The prevalence and size of hernias in patients with Barrett's esophagus was investigated. METHODS: Axial hernia length and the width of the diaphragmatic hiatus were measured prospectively at endoscopy. RESULTS: A 2-cm or longer hernia was found in 96% of 46 patients with Barrett's esophagus, in 42% of 103 controls (p < 0.001), and in 72% of 18 patients with short segment Barrett's esophagus (p < 0.05 vs controls). A hernia was found in 71% of 31 controls with esophagitis and in 29% of 72 controls without esophagitis (p < 0.001). Of 54 controls with neither esophagitis or reflux symptoms, 20% had a hernia. Mean hernia length was 3.95 cm in Barrett's esophagus, and 2.81 cm in controls (p < 0.005). Mean hiatus width was 3.52 cm in patients with Barrett's esophagus and hernia, and 2.24 cm in controls with hernia. Hernia length was similar in patients with and without esophagitis, and in short segment Barrett's esophagus. CONCLUSIONS: Most patients with Barrett's esophagus have hiatal hernia; their hernias are longer and the hiatal openings wider than in controls with or without esophagitis. Hiatal hernia likely contributes to the development of Barrett's esophagus.     

Barrett's esophagus: prevalence and its relationship with dyspeptic symptoms

BACKGROUND AND AIM: Barrett's metaplasia is a premalign condition which plays a pivotal role in the development of esophageal adenocarcinoma. It is considered a complication of chronic gastroesophageal reflux disease. Although esophageal adenocarcinoma is an uncommon cancer, its incidence is rapidly increasing. The aims of the present study were to determine the prevalence of Barrett's metaplasia in outpatients referred for gastroscopy for upper gastrointestinal symptoms, and to clarify the relationship between Barrett's metaplasia and upper gastrointestinal symptoms. METHODS: Three-hundred and ninety-five consecutive dyspeptic patients, never previously investigated, underwent gastroscopy and were enrolled into the study. RESULTS: Barrett's metaplasia was detected in 29 patients (7.4%). The age-specific prevalence of Barrett's metaplasia increased with age. In multivariate analysis, Barrett's metaplasia was independently and positively related to age, sex and duration of symptoms, but not with upper gastrointestinal symptoms. In univariate analysis, Barrett's metaplasia was significantly more common in patients with antral intestinal metaplasia (24%) and presence of hiatal hernia (65.5%), compared with those with normal endoscopic findings (6.2% and 39.2%, respectively, p = 0.001). CONCLUSION: Symptoms do not predict Barrett's metaplasia. Barrett's metaplasia is age-related and more common in patients with a longer duration of symptoms, presence of hiatal hernia and antral intestinal metaplasia.     

Barrett's esophagus: incidence and prevalence estimates in a rural Mid-Western population

BACKGROUND AND AIMS: Barrett's esophagus (BE) predisposes to adenocarcinoma of the esophagus and survival in esophageal adenocarcinoma is low. We studied patients diagnosed with BE in the Marshfield Epidemiologic Study Area (MESA). Our objectives were to estimate the prevalence of diagnosed BE, estimate the annual incidence of initial diagnosis of BE, and characterize the demographics of patients diagnosed with BE. METHODS: We retrospectively reviewed medical records of patients diagnosed with BE until December 31, 2002. The esophagogastroduodenoscopy (EGD) reports were reviewed to establish the presence of columnar epithelium. All slides were retrieved and reviewed by a gastrointestinal pathologist to establish the presence of intestinal metaplasia and dysplasia. Chart abstraction was conducted using a standardized form. RESULTS: BE was histologically confirmed in 216 patients. All were white, 165 (76%) were male, and 81% had a hiatal hernia. Median age at diagnosis was 65.5 yr (range 17-94). Long-segment BE (LSBE) was present in 112 (51.9%) patients. The prevalence of histologically confirmed BE in MESA was 261.8 (95% CI 222.5-301.1) per 100,000 people. The incidence of an initial diagnosis of BE between 1996 and 2002 was 32.7 per 100,000 person-years (95% CI 27.1-38.2) and did not change significantly over the study period despite an increase in EGD rates. At the initial diagnosis, 41.7% of the patients were on proton pump inhibitors. Dysplasia was present in 24.5% of patients. CONCLUSION: The incidence of initial diagnosis of BE in a stable white population did not change significantly over a 7-yr period, despite an increase in EGD rates.     

Preoperative prevalence of Barrett's esophagus in esophageal adenocarcinoma: a systematic review.

BACKGROUND & AIMS: The public health impact of past screening and surveillance practices on the outcomes of Barrett's related cancers has not previously been quantified. Our purpose was to determine the prior prevalence of Barrett's esophagus in reported cases of incident adenocarcinoma undergoing resection, as an indirect measure of impact. METHODS: We performed a systematic review of the literature from 1966 to 2000. Studies were included if they reported: (1) the number of consecutive adenocarcinomas resected, and (2) the number of those resected who had a previously known diagnosis of Barrett's. We generated summary estimates using a random effects model. RESULTS: We identified and reviewed 752 studies. Twelve studies representing a total of 1503 unique cases of resected adenocarcinomas met inclusion criteria. Using a random effects model, the overall percentage of patients undergoing resection who had a prior diagnosis of Barrett's was 4.7% +/- 2.9%. CONCLUSIONS: The low prior prevalence (approximately 5%) of Barrett's esophagus in this study population provides indirect evidence to suggest that recent efforts to identify patients with Barrett's-whether through endoscopic screening or evaluation of symptomatic patients-have had minimal public health impact on esophageal adenocarcinoma outcomes. The potential benefits of endoscopic surveillance seem to have been limited to only a fraction of those individuals at risk. These data thus provide a clear and compelling rationale for the development of effective screening strategies to identify patients with Barrett's esophagus.     

Barrett's esophagus

Barrett's oesophagus is a premalignant metaplastic change of the oesophageal mucosa. Due to its relationship with oesophageal reflux disease and the development of adenoma-carcinoma of the oesophagus the problem arouses increasing interest. In the wide pathogenesis of the disease most probably the composite effect of the refluxed HCl content and duodenal juices play a part. In the diagnosis in addition to fundamental methods--endoscopy and histology--increasingly chromoendoscopy and fluorescent endoscopy are involved. Dispensarization of patients is essential and depends on the degree of pathohistological epithelial changes. Treatment of Barrett's oesophagus can be divided into conservative, where the drug of choice are proton pump inhibitors, and surgical treatment. Promising is endoscopic ablation of the epithelium in combination with subsequent antisecretory therapy.     

Barrett's esophagus

Barrett's esophagus is an acquired condition resulting from severe esophageal mucosal injury. It still remains unclear why some patients with gastroesophageal reflux disease develop Barrett's esophagus whereas others do not. The diagnosis of Barrett's esophagus is established if the squamocolumnar junction is displaced proximal to the gastroesophageal junction and if intestinal metaplasia is detected by biopsy. Despite this seemingly simple definition, diagnostic inconsistencies remain a problem, especially in distinguishing short segment Barrett's esophagus from intestinal metaplasia of the gastric cardia. Barrett's esophagus would be of little importance were it not for its well-recognized association with adenocarcinoma of the esophagus. The incidence of esophageal adenocarcinoma continues to increase and the 5-year survival rate for this cancer remains dismal. However, cancer risk for a given patient with Barrett's esophagus is lower than previously estimated. Current strategies for improved survival in patients with esophageal adenocarcinoma focus on cancer detection at an early and potentially curable stage. This can be accomplished either by screening more patients for Barrett's esophagus or with endoscopic surveillance of patients with known Barrett's esophagus. Current screening and surveillance strategies are inherently expensive and inefficient. New techniques to improve the efficiency of cancer surveillance are evolving rapidly and hold the promise to change clinical practice in the future. Treatment options include aggressive acid suppression, antireflux surgery, chemoprevention, and ablation therapy, but there is still no clear consensus on the optimal treatment for these patients.     

Barrett's esophagus

Barrett's esophagus is an acquired metaplastic abnormality in which the normal stratified squamous epithelium lining of the esophagus is replaced by an intestinal-like columnar epithelium. While in itself a benign and asymptomatic disorder, the clinical importance of this relatively common condition relates to its role as a precursor lesion to esophageal adenocarcinoma, the incidence of which has dramatically increased in Western populations in recent years. Although known to arise as a consequence of chronic gastroesophageal reflux, the cellular and molecular mechanisms underlying development Barrett's esophagus and its progression to cancer remain unclear.     

Barrett's esophagus: age, prevalence, and extent of columnar epithelium.

The development of Barrett's esophagus was studied using data from 51,311 patients undergoing upper gastrointestinal endoscopy between 1976 and 1989. Three hundred seventy-seven patients had greater than or equal to 3-cm columnar epithelium in the esophagus and no carcinoma. The prevalence of Barrett's esophagus increased with age to reach a plateau by the seventh decade. Half of the maximum prevalence was reached by age 40 years, the estimated median age of development of the disorder. Unlike prevalence, the mean length of columnar epithelium did not increase with age. No significant change in length was found in 21 patients followed up for a mean of 7.3 years (mean initial length, 8.29 +/- 0.85 cm; mean final length, 8.33 +/- 0.77 cm). The length of columnar epithelium did not increase in the presence of esophagitis or decrease when esophagitis was absent. Mean age at diagnosis of Barrett's esophagus was 63 years without carcinoma and 64 years in a separate group of patients with adenocarcinoma. The data are consistent with a fairly rapid evolution of Barrett's esophagus to its full length with little subsequent change. Barrett's esophagus may develop more than 20 years before the mean age of clinical recognition or the development of esophageal adenocarcinoma.     

Barrett's esophagus: a review

Barrett's esophagus may be defined as a columnar epithelium-lined distal esophagus. As a frequently recognized complication of gastroesophageal reflux, Barrett's esophagus has become a diagnosis of general clinical concern. Factors governing the development of this complication in patients with gastroesophageal reflux are unknown but may be congenitally determined in part. When symptoms are present, they are due to the complications of reflux, such as esophagitis, stricture, ulcer, or bleeding. Barrett's esophagus may be suspected on the basis of results of a barium meal test, endoscopy, or isotope scanning. Iodine staining at endoscopy or manometrically guided biopsy helps to localize the abnormal mucosal segment. The diagnosis is proved by biopsy. The columnar epithelium of Barrett's esophagus has a malignant predisposition, and, once the diagnosis is made, periodic endoscopy, with biopsy and cytologic study, is indicated. The treatment of Barrett's esophagus is directed toward objective cessation of gastroesophageal reflux. In refractory cases, antireflux surgery improves symptoms and complications from reflux, but the columnar epithelium generally persists along with its malignant potential. It is not known whether effective antireflux treatment will lower the incidence of adenocarcinoma.     

Barrett食管的临床研究

目的研究Barrett食管(Barrett's     

Barrett's esophagus: clinical characteristics

Barrett's metaplasia develops in 6-14% of individuals with gastroesophageal reflux. Barrett's adenocarcinomas are increasing in epidemic proportions for as yet unknown reasons, approximately 0.5-1% of patients with Barrett's will develop adenocarcinoma. Heartburn duration and frequency (but not severity), male gender, and Caucasian race are major risk factors for developing cancer. Obesity and smoking are weak risk factors. Survival is determined by depth of tumor invasion (stage). Once invasion of the muscularis propia occurs, the vast majority of patients will have developed widespread metastasis, even when clinical staging studies are negative. No currently available therapy results in prolonged survival once metastases develop. Thus, the more widespread use of effective surveillance strategies is the only currently available means for reducing the morbidity and mortality associated with Barrett's adenocarcinoma.