Clinical, endoscopic, and functional studies in 408 patients with Barrett's esophagus, compared to 174 cases of intestinal metaplasia of the cardia

OBJECTIVE: The pathophysiology of gastroesophageal reflux disease (GERD) has been studied extensively in patients with long-segment Barrett's esophagus (LSBE), but few reports have explored GERD pathophysiology in patients who have short-segment Barrett's esophagus (SSBE) or intestinal metaplasia at the cardia (IMC). We aimed to compare clinical, endoscopic, histological, and functional features in patients with LSBE, SSBE, and IMC. METHODS: We identified 582 patients who had intestinal metaplasia at the squamocolumnar junction in the distal esophagus and divided them into three groups based on the extent of columnar-lined esophagus observed endoscopically: 1) patients with IMC who had no columnar-lined esophagus (i.e., the squamocolumnar and gastroesophageal junctions coincided), 2) patients with LSBE who had >3 cm of columnar-lined esophagus, and 3) patients with SSBE who had <3 cm of columnar-lined esophagus. All patients had esophageal manometric evaluation, and 24-h esophageal pH monitoring was performed to determine the extent of acid and bile (bilirubin) reflux. RESULTS: There were 174 patients with IMC, 155 with LSBE, and 25 with SSBE. Compared to patients with LSBE and SSBE, patients with IMC had significantly lower frequencies of GERD symptoms, hiatal hernia, and erosive esophagitis; significantly higher lower esophageal sphincter pressures; and significantly shorter durations of acid and bile reflux. Between patients with SSBE and LSBE, significant differences were found in the frequency of hiatal hernia and duration of acid reflux (both greater in the patients with LSBE). Also, dysplasia was significantly more frequent in patients with LSBE than in those with SSBE or IMC. CONCLUSION: GERD symptoms, signs, and physiological abnormalities are found more often in patients with Barrett's esophagus than in those with IMC, and the duration of acid reflux in patients with LSBE is greater than that in patients with SSBE. These findings suggest that the extent of intestinal metaplasia in the esophagus is related directly to the severity of underlying GERD.     

CagA-positive strains of Helicobacter pylori may protect against Barrett's esophagus

OBJECTIVE: Helicobacter pylori (H. pylori) colonization is associated with chronic gastritis, peptic ulcer disease, and adenocarcinoma of the distal stomach. However, the role of H. pylori strain variation in complicated gastroesophageal reflux disease, especially Barrett's esophagus, is unknown. Therefore, the aim of this study was to evaluate the prevalence of colonization by cagA+ and cagA- H. pylori strains in the spectrum of gastroesophageal reflux disease, including Barrett's esophagus. METHODS: A total of 251 patients undergoing endoscopy were categorized into four groups: controls, patients with gastroesophageal reflux disease alone, and patients with short- and long-segment Barrett's esophagus. All patients underwent upper endoscopies with biopsies and serum collections. H. pylori and degree of mucosal inflammation in gastric biopsies were assessed and serological assessment made for H. pylori and cagA status. RESULTS: The overall prevalence of H. pylori colonization in the study population was 35% (95% confidence interval = 29.5-41.4%) which did not differ significantly among the groups. However, colonization by cagA+ H. pylori strains was significantly more prevalent among controls (11/25; 44%) and patients with gastroesophageal reflux disease (13/36; 36%) than in patients with short-segment (2/10; 20%) or long-segment Barrett's esophagus (0/18; 0%). Patients with Barrett's esophagus were less likely to be colonized by cagA+ H. pylori strains than reflux patients without Barrett's esophagus (odds ratio = 0.27, 95% confidence interval = 0.11-0.67, p = 0.004). CONCLUSIONS: Colonization by cagA+ H. pylori strains may be protective against the formation of short- and long-segment Barrett's esophagus and its malignant complications.     

Gastric surgery is not a risk for Barrett's esophagus or esophageal adenocarcinoma.

BACKGROUND & AIMS: The contribution of duodeno-gastroesophageal reflux to the development of Barrett's esophagus has remained an interesting but controversial topic. The present study assessed the risk for Barrett's esophagus after partial gastrectomy. METHODS: The data of outpatients from a medicine and gastroenterology clinic who underwent upper gastrointestinal endoscopy for any reason were analyzed in a case-control study. A case population of 650 patients with short- segment and 366 patients with long-segment Barrett's esophagus was compared in a multivariate logistic regression to a control population of 3047 subjects without Barrett's esophagus or other types of gastroesophageal reflux disease. RESULTS: In the case population, 25 (4%) patients with short-segment and 15 (4%) patients with long-segment Barrett's esophagus presented with a history of gastric surgery compared with 162 (5%) patients in the control population, yielding an adjusted odds ratio of 0.89 with a 95% confidence interval of 0.54-1.46 for short-segment and an adjusted odds ratio of 0.71 (0.30-1.72) for long-segment Barrett's esophagus. Similar results were obtained in separate analyses of 64 patients with Billroth-1 gastrectomy, 105 patients with Billroth-2 gastrectomy, and 33 patients with vagotomy and pyloroplasty for both short- and long-segment Barrett's esophagus. Caucasian ethnicity, the presence of hiatus hernia, and alcohol consumption were all associated with elevated risks for Barrett's esophagus. CONCLUSIONS: Gastric surgery for benign peptic ulcer disease is not a risk factor for either short- or long-segment Barrett's esophagus. This lack of association between gastric surgery and Barrett's esophagus suggests that reflux of bile without acid is not sufficient to damage the esophageal mucosa.     

Cytokeratin immunoreactivity patterns in the diagnosis of short-segment Barrett's esophagus

BACKGROUND & AIMS: The origin of intestinal metaplasia in short segments of columnar mucosa at the esophagogastric junction has clinical importance but can be difficult to determine at endoscopy. Cytokeratin (CK) 7 and 20 patterns are specific for long-segment Barrett's esophagus; however, their utility in short-segment Barrett's esophagus has not been assessed. METHODS: Endoscopic biopsy specimens from patients with long-segment Barrett's esophagus (n = 49), suspected short-segment Barrett's esophagus (n = 43), and gastric intestinal metaplasia (n = 26) were immunostained for CK7 and CK20. Comprehensive clinical data were obtained, including age, gender, and hiatal hernia and Helicobacter pylori status. RESULTS: A Barrett's CK7/20 pattern was present in 48 (98%) of 49 patients with long-segment Barrett's esophagus, 35 (82%) of 43 with suspected short-segment Barrett's esophagus, and 0 (0%) of 26 patients with gastric intestinal metaplasia. Patients with suspected short-segment Barrett's esophagus with a Barrett's CK7/20 pattern were clinically similar to those with long-segment Barrett's esophagus. In contrast, patients with suspected short-segment Barrett's esophagus with no Barrett's CK7/20 pattern were clinically similar to those with gastric intestinal metaplasia. CONCLUSIONS: A Barrett's CK7/20 pattern identifies a subset of patients with suspected short-segment Barrett's esophagus who have a patient profile similar to that seen in long-segment Barrett's esophagus. A Barrett's CK7/20 pattern is an objective marker of Barrett's mucosa that in conjunction with appropriate clinical and endoscopic data can be used by clinicians to better define patients with short-segment Barrett's esophagus.     

Specialized intestinal metaplasia of the distal esophagus in gastroesophageal reflux disease: prevalence and clinico-demographic features

BACKGROUND: Specialized intestinal metaplasia can be categorized according endoscopic and histological findings in long segment Barrett, short segment Barrett and specialized intestinal metaplasia of cardia. Barrett's esophagus is an acquired disease that is found in about 10%-13% of patients undergoing endoscopy for symptoms of gastroesophageal reflux disease and it is well established as predisposing to esophageal adenocarcinoma. The columnar epithelium with goblet cells replaces the normal squamous epithelium. OBJECTIVE: To determine the prevalence and clinical-demographic characteristics of specialized intestinal metaplasia of distal esophagus in the gastroesophageal reflux disease. METHODS: From April to October 2002, 402 patients referred to upper endoscopy due gastroesophageal reflux disease were evaluated through of a symptom questionnaire about clinical and demographic features and submitted to upper endoscopy with four-quadrant biopsies 1 cm below escamocolumnar junction. RESULTS: Eighteen point four percent of patients had specialized intestinal metaplasia, 0.5% long segment Barrett esophagus, 3.2% short segment Barrett's esophagus and 14.7% specialized intestinal metaplasia of cardia. Patients with Barrett's esophagus showed a tendency to be male and specialized metaplasia of cardia to be female. All patients with Barrett's esophagus were white. There was not association between symptoms of gastroesophageal reflux disease and specialized intestinal metaplasia, but patients with Barrett's esophagus showed a tendency to have symptoms over 5 years and had more hiatal hernia and esophagitis. The use of alcohol and tobacco was not related to the presence of specialized intestinal metaplasia. CONCLUSIONS: Barrett's esophagus was more related to the male gender, gastroesophageal reflux disease symptoms for 5 years or longer, more intense esophagitis and hiatal hernia, but was not related to the use of tobacco and alcohol.     

Is Barrett's esophagus characterized by more pronounced acid reflux than severe esophagitis?

Objective: Barrett's esophagus is related to gastroesophageal reflux disease (GERD). However, only a small fraction of patients with GERD develop Barrett's esophagus. We evaluated whether gastroesophageal acid reflux is more pronounced in Barrett's patients than in patients with moderate or severe endoscopic esophagitis.
Methods: Retrospective evaluation of results of esophageal manometry and 24 hour ambulatory pH monitoring performed between 1990 and 1996 at the Leiden University Medical Center in those patients who also underwent endoscopy ≤3 months before pH-metry. Included were 51 patients with Barrett's esophagus, 30 patients with severe esophagitis, 45 patients with moderate esophagitis, and 24 healthy control subjects.
Results: Patients with Barrett's esophagus had significantly increased acid reflux time (   p < 0.01  –0.05) compared to patients with moderate, but not compared to patients with severe esophagitis. Distal esophageal body motility and LES pressure were significantly (   p < 0.01  –0.05) reduced in patients with Barrett's esophagus compared to patients with moderate esophagitis but not compared to those with severe esophagitis.
Conclusion: Although acid reflux is increased in patients with Barrett's esophagus and esophageal motility is impaired, other factors apart from acid exposure and motility contribute to the development of Barrett's esophagus.     

The Prevalence of Intestinal Metaplasia in Patients With and Without Peptic Strictures

Objective: Several studies suggest that patients with esophageal peptic strictures have a high prevalence of Barrett's esophagus. However, these studies did not include appropriate control groups, were retrospective in nature, or did not strictly define Barrett's esophagus. Our aim was to compare the prevalence of Barrett's esophagus in patients with and without gastroesophageal reflux disease strictures in a prospective study.
Methods: Seventy-nine patients referred for endoscopy for gastroesophageal reflux disease symptoms were evaluated. We collected demographic information and an esophageal symptom assessment. Biopsy specimens were obtained from peptic strictures, Schatzki rings, or from any areas of columnar-lined esophagus or mucosal injury. Barrett's esophagus was strictly defined as the presence of intestinal metaplasia from tubular esophagus.
Results: There were 46 patients without strictures and 28 patients with peptic strictures. Five patients had Schatzki's rings. The prevalence of intestinal metaplasia was 23.9% in patients without strictures, and 25% in patients with peptic strictures ( p = NS ). There was no difference in prevalence of short- or long-segment Barrett's esophagus between the groups. Patients with strictures were older than patients without strictures (mean age 58.9 vs 48.6 yr), and more likely to have mucosal injury (50% vs 26.1%). Otherwise, there were no significant differences with regards to gender, race, heartburn duration or frequency.
Conclusions: Barrett's esophagus, as defined by the presence of intestinal metaplasia in the tubular esophagus, is equally common in patients with and without peptic strictures. There does not appear to be an association between Barrett's esophagus and peptic strictures.     

Capsaicin induction of esophageal symptoms in different phenotypes of gastroesophageal reflux disease

"Background: Type 1 vanilloid receptors (TRPV1) have been described on esophageal afferent sensitive neurons. Stimulation of TRPV1 receptors with capsaicin may induce heartburn. Capsaicin is the pungent component of chili and the most extensively studied TRPV1 agonist. Objectives: To investigate the effect of esophageal stimulation with intraesophageal capsaicin administration on induction of esophageal symptoms and on esophageal chemo-sensitization to acid in different gastroesophageal reflux disease (GERD) phenotypes. Methods: Healthy volunteers and patients with GERD (non-erosive [NERD], erosive GERD [EE] and Barrett's esophagus [BE]) were prospectively studied. All subjects were randomized to receive either intraesophageal perfusion capsaicin or saline 0.9%. Thirty minutes after saline or capsaicin infusion an acid perfusion test of HCl was performed. A week later, a crossover phase with capsaicin versus saline was performed. Five symptoms were evaluated every 5 min during the first 30 minutes after capsaicin, saline, and acid perfusion: chest burning, chest pain, heartburn, epigastric burning, and epigastric pain Results: 17 healthy subjects and 31 GERD patients (10 NERD, 11 EE, and 10 BE) were included. Twenty- eight (90%) of GERD and 6 (35%) of healthy subjects had esophageal symptoms after capsaicin perfusion. Mean for the 5 evaluated symptoms induced by capsaicin was significantly higher in the GERD group compared to the control group. The highest symptom severity was in the erosive subgroup. Capsaicin decreased the 5 symptoms induced by acid perfusion in both healthy volunteers and GERD patients. Total score of esophageal symptom severity (produced by acid perfusion) was significantly reduced by capsaicin infusion in the BE group. Conclusions: Capsaicin induces esophageal and gastric symptoms in healthy volunteers and GERD patients. Capsaicin reduces esophageal chemosensitivity to acid, especially in patients with BE. "     

Capsule endoscopy for screening for short-segment Barrett's esophagus

BACKGROUND: The rise in the incidence of esophageal adenocarcinoma has led to the development of new methods to screen for the precursor lesion, Barrett's esophagus. AIM: To evaluate the potential role of esophageal capsule endoscopy in identifying the presence of short-segment Barrett's esophagus. METHODS: Patients with biopsy-proven short-segment Barrett's esophagus underwent esophageal capsule endoscopy. The images were reviewed by two expert observers with no knowledge of the purpose of the study. The data collected included transit time, quality of image, presence or absence of Z-line, Schatzki's ring, hiatal hernia, and Barrett's esophagus (long or short, definite or suspected). RESULTS: Twenty patients were studied; in 18, the capsule passed into the stomach. Barrett's esophagus was identified or suspected in eight cases (44%) by one observer and three (16%) by the second (P= 0.14). Although the Z-line was seen in the 18 cases that were qualified by both observers, there was an agreement in only six cases as to whether it was regular or irregular. Erosive gastroesophageal reflux disease (GERD) was scored as present in three and absent in six patients by both readers. Nonexisting feline esophagus, varices, and distal esophageal stricture were suspected in one patient each. CONCLUSIONS: Esophageal capsule endoscopy had a high interobserver variability and a low yield for short-segment Barrett's esophagus. Esophageal capsule endoscopy cannot be recommended for screening for short-segment Barrett's esophagus.     

The frequency of Barrett's esophagus in high-risk patients with chronic GERD

BACKGROUND: The reported frequency of Barrett's esophagus (BE) in patients with reflux symptoms varies from 5% to 15%. The exact frequency of long-segment BE (LSBE) (>3 cm) and short-segment BE (SSBE) (<3 cm) in patients with chronic symptoms of GERD is uncertain. The aim of this study was to determine the frequency of LSBE and SSBE in consecutive patients presenting for a first endoscopic evaluation with GERD as the indication. METHODS: Consecutive patients presenting to the endoscopy unit of a Veterans Affairs Medical Center for a first upper endoscopy with the indication of GERD were prospectively evaluated. Demographic information (gender, race, age), data on tobacco use and family history of esophageal disease, and body mass index (BMI) were recorded for all patients. Before endoscopy, all patients completed a validated GERD questionnaire. The diagnosis of BE was based on the presence of columnar-appearing mucosa in the distal esophagus, with confirmation by demonstration of intestinal metaplasia in biopsy specimens. All patients with erosive esophagitis on the initial endoscopy underwent a second endoscopy to document healing and to rule-out underlying BE. Patients with a history of BE, alarm symptoms (dysphagia, weight loss, anemia, evidence of GI bleeding), or prior endoscopy were excluded. RESULTS: A total of 378 consecutive patients with GERD (94% men, 86% white; median age 56 years, range 27-93 years) were evaluated. A diagnosis of BE was made in 50 patients (13.2%). The median length of Barrett's esophagus (BE) was 1.0 cm (range 0.5-15.0 cm). Of the patients with BE, 64% had short-segment BE (SSBE) (overall SSBE frequency 8.5%). The overall frequency of long-segment BE (LSBE) was 4.8%. A hiatal hernia was detected in 62% of the patients with BE. Of the 50 patients with BE (median age 62 years, range 29-81 years), 47 (94%) were men and 98% were white. Eighteen patients (36%) were using tobacco at the time of endoscopy; 23 (46%) were former users. The median body mass index (BMI) of patients with BE was 27.3 (overweight). There were no significant differences between patients with LSBE and SSBE with respect to age, gender, ethnicity, BMI, and GERD symptom duration. CONCLUSIONS: The frequency of BE in a high-risk patient group (chronic GERD, majority white men, age > 50 years) who sought medical attention is 13.2%, with the majority (64%) having SSBE. These data suggest that the frequency of BE in patients with GERD has not changed. The true prevalence of BE in the general population, including those who do not seek care, is undoubtedly lower, currently and historically. The majority of patients with BE are overweight and have a hiatal hernia. Demographic data for patients with LSBE and SSBE are similar, indicating that these are a continuum of the same process.     

Cytokeratin immunoreactivity patterns in short-segment Barrett's esophagus in Japanese patients

BACKGROUND: The origin of intestinal metaplasia at the esophagogastric junction has clinical importance. However, it can be difficult to differentiate between intestinal metaplasia of short-segment Barrett's esophagus and cardiac intestinal metaplasia due to Helicobacter pylori infection. Specific patterns of cytokeratin (CK)7 and CK20 have been detected in long-segment Barrett's esophagus. The aim of the present study was to assess the immunostaining patterns associated with short-segment Barrett's esophagus. AIMS: Paraffin-embedded biopsy specimens were prepared from 128 patients with intestinal metaplasia of long-segment Barrett's esophagus (n = 3), short-segment Barrett's esophagus without H. pylori infection (n = 22), short-segment Barrett's esophagus with H. pylori infection (n = 22), and cardiac mucosa (n = 49) and gastric mucosa from antrum and fundus (n = 44) with H. pylori infection. Sections were prepared and immunostained for CK7 and CK20. RESULT: A Barrett's CK7/20 pattern was present in all three patients (100%) with long-segment Barrett's esophagus, 21 of 22 patients (95%) with short-segment Barrett's esophagus without H. pylori infection, and six of 22 patients (27%) with short-segment Barrett's esophagus with H. pylori infection (P < 0.05). CONCLUSION: Intestinal metaplasia of short-segment Barrett's esophagus in patients without H. pylori infection is thought to be similar to that seen in long-segment Barrett's esophagus.     

Hiatal Hernia and Acid Reflux Frequency Predict Presence and Length of Barrett's Esophagus

One third of the general population may experience reflux symptoms, yet only a small fraction of patients with gastroesophageal reflux disease (GERD) have Barrett's esophagus. The aim of the present study was to compare the characteristics of GERD patients with and without Barrett's esophagus and identify potential risk factors for the appearance of Barrett's esophagus in reflux disease. Outpatients from a gastroenterology clinic who underwent upper gastrointestinal endoscopy, esophageal manometry, and 24-hr pH monitoring were recruited into a case-control study. A total of 256 case subjects with endoscopically and histologically proven Barrett's esophagus were compared to a control group of 229 subjects with nonerosive reflux disease. As compared to nonerosive reflux disease, Barrett's esophagus was strongly associated with more reflux episodes. Barrett's esophagus occurred more frequently among subjects with hiatus hernia and among subjects who consumed large amounts of alcohol or cigarettes. Frequent reflux episodes, hiatus hernia, smoking, and alcohol consumption were also risk factors for an increased length of Barrett's mucosa. Total esophageal mucosal acid contact time at pH < 4 was a significant risk factor for the length but not the presence of Barrett's esophagus. Intake of aspirin or NSAIDs was similar in patients with and without Barrett's esophagus. In conclusion, in comparison with nonerosive reflux disease, Barrett's esophagus is characterized by risk factors usually indicative of severe types of GERD. Mechanisms in addition to acid reflux must contribute to the development of Barrett's esophagus.     

Esophageal perforation at a Barrett's ulcer

An alcoholic man with known reflux esophagitis and Barrett's esophagus developed fever, epigastric pain, subcutaneous crepitus, and leukocytosis from an esophageal perforation at a Barrett's ulcer. Possible risk factors for perforation in this patient included alcoholism, severe gastroesophageal reflux, corticosteroid therapy, noncompliance with antacid and H2 blocker therapy, and the presence of acid-secreting parietal cells in the Barrett's epithelium. Five cases of this complication have previously been reported in a review of the literature, which included 536 cases of Barrett's esophagus or esophageal perforation. This entity may present with a clinical triad of a patient (a) in acute distress with fever and epigastric or noncardiac chest pain and without signs of peritonitis, (b) with symptoms of or known gastroesophageal reflux, and (c) with chest examination revealing subcutaneous crepitus, or chest roentgenogram revealing subcutaneous emphysema, pneumomediastinum, or hydropneumothorax.     

Barrett＇s esophagus： Prevalence and risk factors in patients with chronic GERD in Upper Egypt

AIM： To determine the prevalence and possible risk factors of Barrett＇s esophagus （BE） in patients with chronic gastroesophageal reflux disease （GERD） in EI Minya and Assuit, Upper Egypt. METHODS： One thousand consecutive patients with chronic GERD symptoms were included in the study over 2 years. They were subjected to history taking including a questionnaire for GERD symptoms, clinical examination and upper digestive tract endoscopy. Endoscopic signs suggestive of columnar-lined esophagus （CLE） were defined as mucosal tongues or an upward shift of the squamocolumnar junction. BF was diagnosed by pathological examination when specialized intestinal metaplasia was detected histologically in suspected CLE. pH was monitored in 40 patients. RESULTS： BE was present in 7.3% of patients with chronic GERD symptoms, with a mean age of 48.3 ± 8.2 years, which was significantly higher than patients with GERD without BE （37.4 ± 13.6 years）. Adenocarcinoma was detected in eight cases （0.8%）, six of them in BE patients. There was no significant difference between patients with BE and GERD regarding sex, smoking, alcohol consumption or symptoms of GERD. Patients with BE had significantly longer esophageal acid exposure time in the supine position, measured by pH monitoring. CONCLUSION： The prevalence of BE in patients with GERD who were referred for endoscopy was 7.3%. BE seems to be associated with older age and more in patients with nocturnal gastroesophageal reflux.     

Esophageal acid sensitivity in Barrett's esophagus

Esophageal acid sensitivity was evaluated in 15 patients with Barrett's esophagus and in 15 patients with reflux esophagitis uncomplicated by Barrett's. Patients with Barrett's esophagus had sensitivity to esophageal acid perfusion less frequently than those with uncomplicated reflux esophagitis (66 vs. 100%; p less than 0.05). Moreover, patients with Barrett's esophagus with acid sensitivity took longer to develop pain during acid perfusion (p less than 0.05), and overall, experienced less severe symptoms (p less than 0.01) than those with reflux esophagitis. Over a 2-week period, as judged by diary, the Barrett's group had less frequent (p less than 0.01) and less severe (p less than 0.01) heartburn symptoms than the other patients. These results indicate that patients with Barrett's esophagus have significantly reduced esophageal acid sensitivity and, as a consequence, have an impaired ability to recognize acid reflux.     

Does methylene blue detect intestinal metaplasia in Barrett's esophagus?

BACKGROUND: Methylene blue has been used to selectively stain areas of specialized intestinal metaplasia in Barrett's esophagus. The sensitivity, specificity, and negative and positive predictive values for the detection of specialized intestinal metaplasia by methylene blue chromoendoscopy were determined in patients with Barrett's esophagus. METHODS: Thirty patients with Barrett's esophagus underwent endoscopy with biopsy specimens obtained from areas that stained positive and negative with methylene blue. Histopathologic findings were compared with methylene blue chromoendoscopy findings. RESULTS: Two hundred ninety-two biopsy specimens (mean 9.7/patient) were obtained: 203 from stained and 89 from unstained areas. Sensitivity, specificity, and negative and positive predictive values for detection of specialized intestinal metaplasia were, respectively, 72%, 46%, 22%, and 89%. Comparing 187 biopsy specimens from patients with long-segment Barrett's esophagus with 105 specimens from patients with short-segment Barrett's esophagus, the sensitivity, specificity, and negative and positive predictive values were, respectively, 77% versus 63% (p = 0.044), 79% versus 21% (p < 0.002), 28% versus 14% (p = 0.219), and 97% versus 73% (p < 0.002). The odds ratio for detection of specialized intestinal metaplasia in stained areas was 12.40 in long-segment and 0.45 in short-segment Barrett's esophagus. CONCLUSIONS: Data from this study confirm the value of methylene blue chromoendoscopy for detection of specialized intestinal metaplasia in long-segment Barrett's esophagus, but not in short-segment Barrett's esophagus.     

Hiatal hernia size,Barrett's length,and severity of acid reflux are all risk factors for esophageal adenocarcinoma

OBJECTIVE: The reasons for the development of dysplasia and adenocarcinoma in Barrett's mucosa are not well understood. The aims of this study were to characterize risk factors for the transition from Barrett's esophagus without dysplasia to Barrett's esophagus with high-grade dysplasia or esophageal adenocarcinoma. METHODS: A group of 131 patients with high-grade dysplasia or esophageal adenocarcinoma were selected as case subjects. A first population of 2170 patients without gastroesophageal reflux disease (GERD) and a second population of 1189 patients with Barrett's esophagus served as two control groups. Logistic regression analyses were used to compare the risk factors associated with the occurrence of high-grade dysplasia or esophageal adenocarcinoma. RESULTS: Patients with high-grade dysplasia or esophageal adenocarcinoma shared many characteristics with other forms of severe GERD, such as older age, male gender, and white ethnicity. The length of Barrett's esophagus and the size of hiatus hernia increased the risk for both conditions. Subjects with high-grade dysplasia and adenocarcinoma had more severe acid reflux than patients with other forms of GERD. Smoking and alcohol consumption did not affect the risk for developing high-grade dysplasia or adenocarcinoma in patients with Barrett's esophagus. CONCLUSIONS: High-grade dysplasia and esophageal adenocarcinoma seem to stem from an extreme and unfavorable constellation of all risk factors that are generally held responsible for the development of GERD and Barrett's esophagus.     

Prevalence of Barrett's esophagus in asymptomatic individuals

BACKGROUND & AIMS: The incidence of esophageal adenocarcinoma in the western world has been linked to chronic heartburn, regurgitation, and the development of the premalignant epithelium of Barrett's esophagus (BE). However, up to 40% of esophageal adenocarcinomas occur in patients without prior reflux symptoms. We prospectively screened for the presence of BE in asymptomatic subjects older than 50 years of age undergoing screening sigmoidoscopy for colorectal cancer. METHODS: Subjects undergoing sigmoidoscopy for colorectal cancer (CRC) screening were invited to undergo upper endoscopy. Exclusion criteria included symptoms of gastroesophageal reflux disease (GERD) more than once a month, use of medications for GERD, or previous endoscopy. BE was classified as long-segment BE (LSBE), short-segment BE (SSBE), and microscopic specialized intestinal metaplasia of the esophagogastric junction (SIM-EGJ). RESULTS: Of 408 potential study candidates, 110 subjects were screened; 9 were women. The mean (+/-SD) age was 61 +/- 9.3 (range, 50-80) years, most of them (73%) Caucasian. Intestinal metaplasia (IM) extending above the EGJ was detected in 27 (25%) subjects; 8 (7%) had LSBE, and 19 (17%) had SSBE. Patients with BE were no more likely to be obese, consumers of tobacco or alcohol, report a family history of GERD, show association with toxic exposure, or use antacids more than once a month, compared with those without BE. CONCLUSIONS: BE was detected in 25% of asymptomatic male veterans older than 50 years of age undergoing screening sigmoidoscopy for CRC.     

Colonization with cagA-positive Helicobacter pylori strains inversely associated with reflux esophagitis and Barrett's esophagus

AIM: The hypothesis that colonization with cagA(+) Helicobacter pylori strains protects against the development of gastroesophageal reflux disease (GERD) and its complications is tested. METHODS: Patients with reflux esophagitis and Barrett's esophagus were studied. Antral biopsy specimens were obtained for detection of H. pylori. A serum sample was obtained for determination of IgG antibodies to H. pylori and to the CagA protein. RESULTS: 736 patients were studied. 118 patients had reflux esophagitis, 36 had Barrett's esophagus, 108 had hiatal hernia without signs of inflammation (the reflux group), and 20 patients had esophageal or stomach cancer. The remaining 454 patients had no signs of GERD. The 262 patients with reflux disease had a significantly lower prevalence of H. pylori (34.9%) than the 454 controls (54.6%; p<0. 001). Among 310 H. pylori-positive patients from whom serum was available, colonization with cagA(+) strains was detected in 59% in the control group versus 35% in the reflux group (p<0.001). Conclusion: Patients with reflux esophagitis and Barrett's esophagus have a significantly lower prevalence of H. pylori colonization than controls, in particular of the cagA(+) type. These data suggest that colonization with cagA(+) H. pylori strains may be protective against the development of GERD Copyright 2000 S. Karger AG, Basel.