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Esophageal Cancer and Barrett's Esophagus, 3E, focuses on these two common and key conditions that affect the esophagus, providing expert guidance to their pathogenesis, cause, prevention, diagnosis and clinical management. Top international names in the field examine each of the many issues involved, using the very latest evidence-based research, and clear, didactic advice allows the reader to understand the best methods of diagnosis and clinical management of each condition – whether early or late stage. Well-illustrated and fully revised to include the latest in ACG/ASG/UEGW guidelines, it is the perfect consultation tool for gastroenterologists and oncologists managing patients with cancer of the esophagus.  It is also ideal for teaching residents and fellows optimum patient management, and for identifying areas requiring future research.

Esophageal acid exposure is important in the pathogenesis of Barrett's esophagus (BE), and possibly in the progression of BE to dysplasia and carcinoma. The aim of this study is to compare the development of dysplasia in BE patients treated with or without proton pump inhibitor (PPI) or histamine 2-receptor antagonist (H2RA). We analyzed prospectively collected data by a single endoscopist on patients with BE in a VA (Veterans Affairs) setting over a 20-yr time period (1981-2000). A pathologist used standard criteria to diagnose BE/dysplasia. Pharmacy information after 1994 was retrieved from a computerized database, and from research files for the period before that. The receipt and the duration of H2RA and/or PPI use was compared between those with and without dysplasia. The incidence of dysplasia was examined in a Kaplan-Meier survival analysis stratified by PPI treatment status, and the risk of dysplasia was examined in a Cox multiple regression analysis controlling for demographic features, length of BE, and the year of BE diagnosis. We analyzed data for 236 unique veteran patients with a mean age at BE diagnosis of 61.5 yr, 86% Caucasian, and 98% male. During 1,170 patient-yr of follow-up, 56 patients developed dysplasia giving an annual incidence rate of 4.7%. Of those, 14 had high-grade dysplasia. The cumulative incidence of dysplasia was significantly lower among patients who received PPI after BE diagnosis than in those who received no therapy or H2RA; log rank test (p < 0.001). Furthermore, among those on PPIs, a longer duration of use was associated with less frequent occurrence of dysplasia. In multivariate analysis, the use of PPI after BE diagnosis was independently associated with reduced risk of dysplasia, hazards ratio: 0.25 (95% CI 0.13-0.47), p < 0.0001. Longer segments of BE and Caucasian race were other independent risk factors for developing dysplasia. In general, similar findings were observed when only cases with high-grade dysplasia were analyzed. These results indicate that PPI therapy is associated with a significant reduction in the risk of developing dysplasia in patients with BE. However, more studies are required to confirm this finding.

Background: Barrett’s oesophagus is a premalignant condition associated with an increased risk for the development of oesophageal adenocarcinoma (ADCA). Previous studies indicated that oxidative damage contributes to the development of ADCA. Objective: To test the hypothesis that bile acids and gastric acid, two components of refluxate, can induce oxidative stress and oxidative DNA damage. Methods: Oxidative stress was evaluated by staining Barrett’s oesophagus tissues with different degrees of dysplasia with 8-hydroxy-deoxyguanosine (8-OH-dG) antibody. The levels of 8-OH-dG were also evaluated ex vivo in Barrett’s oesophagus tissues incubated for 10 min with control medium and medium acidified to pH 4 and supplemented with 0.5 mM bile acid cocktail. Furthermore, three oesophageal cell lines (Seg-1 cells, Barrett’s oesophagus cells and HET-1A cells) were exposed to control media, media containing 0.1 mM bile acid cocktail, media acidified to pH 4, and media at pH 4 supplemented with 0.1 mM bile acid cocktail, and evaluated for induction of reactive oxygen species (ROS). Results: Immunohistochemical analysis showed that 8-OH-dG is formed mainly in the epithelial cells in dysplastic Barrett’s oesophagus. Importantly, incubation of Barrett’s oesophagus tissues with the combination of bile acid cocktail and acid leads to increased formation of 8-OH-dG. An increase in ROS in oesophageal cells was detected after exposure to pH 4 and bile acid cocktail. Conclusions: Oxidative stress and oxidative DNA damage can be induced in oesophageal tissues and cells by short exposures to bile acids and low pH. These alterations may underlie the development of Barrett’s oesophagus and tumour progression.

ONE of the most important features of non-A, non-B hepatitis is the frequency with which chronic liver disease develops. Most studies of chronic non-A, non-B hepatitis have been follow-up studies of patients who have received transfusions. An average of 50 percent of these patients were shown to have persistently elevated serum aminotransferase levels, and of those who underwent liver biopsy, 60 percent had chronic active hepatitis and 10 to 20 percent had cirrhosis. 1 Only a few studies have examined the rate and severity of chronic liver disease in patients who did not acquire their infections from blood transfusions. 2 3 4 5 6 7 In these . . .

Esophageal capsule endoscopy (ECE) is a novel technique that offers noninvasive evaluation of esophageal pathology in gastroesophageal reflux disease (GERD) patients. To assess the diagnostic accuracy of ECE for Barrett's esophagus (BE), erosive esophagitis, and hiatal hernia and to assess the safety profile of ECE. Patients with GERD symptoms and those undergoing BE surveillance were prospectively enrolled. All patients underwent ECE followed by standard upper endoscopy. ECE findings were interpreted by examiners blinded to endoscopy results. The gold standard was the findings at endoscopy and ECE results were compared with those at endoscopy. One hundred patients were enrolled of which 94 completed the study. At upper endoscopy, BE was suspected in 53 (mean length 3.1 cm) and confirmed in 45 patients. Erosive esophagitis and hiatal hernia were identified in 18 and 70 patients, respectively. The sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of ECE for BE in GERD patients were 67%, 87%, 60%, and 90%, respectively. The sensitivity, specificity, PPV, and NPV of ECE for BE patients undergoing surveillance were 79%, 78%, 94%, and 44%, respectively. The sensitivity, specificity, PPV, and NPV for erosive esophagitis were 50%, 90%, 56%, and 88% and for hiatal hernia were 54%, 67%, 83%, and 33%, respectively. Current diagnostic rates of ECE for BE are not yet accurate enough for application in clinical practice. An improvement in technology and learning curve assessments are required, until then standard upper endoscopy remains the gold standard.

ObjectiveIt is unclear whether Barrett's oesophagus (BO) length changes over time or whether the full length of the segment is established at the onset of disease recognition. The objectives of this study were to evaluate the association of age and BO length and to evaluate the changes in BO length over time.DesignThis is a prospective, multicentre cohort study involving patients with BO from five centres. Patients were divided into groups based on the decade of initial diagnosis of BO. The mean BO length and the mean change in BO length were calculated for each age decade. The mean change in BO length was also calculated between the index endoscopy and the last surveillance endoscopy.Results3635 patients with BO were included in the study: 87.8% men, 92.8% Caucasians, mean age 60.9 years and mean BO length 3.5 cm. The mean change in BO length was 0.9 cm. The mean BO length did not significantly change for each age category: <30 years (4.6 cm), 30–39.9 years (3.2 cm), 40–49.9 years (3.1 cm), 50–59.9 years (3.1 cm), 60–69.9 years (3.6 cm), 70–79.7 (4.0 cm) and >80 years (4.5 cm), p=0.47. On subgroup analysis of patients with non-dysplastic BO who had at least 1 year of endoscopic follow up, there was a significant decrease in mean change in BO length across age categories ranging from +1.7 to −0.8 cm, p=0.03.ConclusionsThere was no significant difference in BO length by age category in decades. In addition, the change in BO length from index to follow-up endoscopy was similar among patients >30 years. These findings suggest that a patient's BO segment length attains its full extent by the time of the initial endoscopic examination.