[Cytologic criteria for the formation of a risk group in Barrett esophagus].
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Oncologic screenings of the populations in the areas with increased incidence of esophageal cancer have revealed Barrett's ulcer in 1 percent of the examinees. Endoscopic and cytologic characteristics of this condition are presented. Precancer changes--severe dysplasia--are most frequent in male Kazakhs (14.1 percent) aged 50 to 59 (14.7 percent). Subjects with Barrett's ulcer developing severe dysplasia, as evidenced by cytograms, should be included in the group of subjects at risk for carcinoma of the lower third of the esophagus and cardia.Keywords:
Barrett's esophagus
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Abstract Esophageal adenocarcinoma develops on a background of Barrett's esophagus. A number of risk factors have been linked to both conditions, including gastroesophageal reflux and smoking. However, the molecular mechanisms by which these factors influence disease progression remain unclear. One possibility is that risk factors generate promutagenic DNA damage in the esophagus. The comet assay was used to measure DNA damage in esophageal (Barrett's and squamous) and gastric mucosa of Barrett's patients with (n = 24) or without (n = 50) associated adenocarcinoma or high-grade dysplasia in comparison with control patients (squamous mucosa) without Barrett's esophagus (n = 64). Patients completed a questionnaire detailing exposure to some of the known risk factors for Barrett's esophagus and adenocarcinoma. In Barrett's esophagus patients, DNA damage was higher in Barrett's mucosa compared with normal esophageal and gastric mucosa (P < 0.001). In addition, the highest quartile of DNA damage in Barrett's mucosa was associated with an increased risk (odds ratio, 9.4; 95% confidence interval, 1.1-83.4; P = 0.044) of developing adenocarcinoma or high-grade dysplasia compared with DNA damage levels in the lowest quartile. Smoking was associated with higher DNA damage in squamous epithelium in all patient groups (P < 0.01) and in Barrett's mucosa (P < 0.05) in Barrett's esophagus patients only. In controls only, current reflux was associated with higher DNA damage, whereas anti-inflammatory drug use resulted in lower levels. Collectively, these data imply a genotoxic insult to the premalignant Barrett's mucosa that may explain the genetic instability in this tissue and the progression to adenocarcinoma. There is an indication for a role for smoking in inducing DNA damage in esophageal mucosa but an understanding of the role of reflux requires further investigation.
Barrett's esophagus
Esophageal disease
Comet Assay
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Abstract: Barrett’s esophagus is the only known precursor lesion for esophageal adenocarcinoma. Previous studies have shown that a variety of methods can be applied to destroy Barrett’s esophagus epithelium, and healing with a new esophageal squamous epithelium usually occurs following ablation. Radiofrequency ablation (RFA) is a relatively new endoscopic technique. It has been claimed that ablation using RFA reduces the risk of cancer progression. RFA is usually easy to apply and is associated with a low risk of morbidity. It achieves complete eradication of (non) dysplastic Barrett’s esophagus in most individuals, and the risk of progression to higher grades of dysplasia or cancer is reduced after RFA, although not completely eliminated. Limitations include recurrence of Barrett’s esophagus in up to one-third of individuals, a risk of “buried islands” of Barrett’s esophagus remaining below the regenerated mucosa, and uncertainty about the biological behavior of the new squamous epithelium after RFA. Current evidence supports the use of RFA in individuals with high-grade dysplasia in Barrett’s esophagus, and early stage (T1a) intramucosal cancer, and select individuals with low-grade dysplasia. As accurate diagnosis of low-grade dysplasia remains difficult outside expert centers, it is probably premature to recommend routine RFA for all patients diagnosed with low-grade dysplasia in the community, despite the favorable outcomes from one randomized trial. Furthermore, long-term outcomes following ablation remain uncertain, and ongoing endoscopy surveillance is still required after RFA as progression to cancer remains a possibility. Outcomes from large studies with long-term follow-up are needed to definitively confirm that RFA ablation can reliably prevent cancer progression in Barrett’s esophagus. Keywords: Barrett’s esophagus, esophageal adenocarcinoma, radiofrequency ablation, dysplasia
Barrett's esophagus
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Barrett's esophagus
Esophageal disease
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Barrett's esophagus
Endoscopic mucosal resection
Surgical oncology
Esophageal adenocarcinoma
Esophageal disease
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Barrett's esophagus (BE) is a well-recognized premalignant condition for development of esophageal adenocarcinoma (EAC). It is defined as the displacement of the squamo-columnar junction proximal to the gastroesophageal junction, with the presence of intestinal metaplasia (IM) on biopsies (Wang and Sampliner 2008; Sharma et al. 2004). Chronic gastroesophageal reflux disease (GERD) is the most frequent identifiable risk factor for Barrett's esophagus (Wang and Sampliner 2008; Sharma et al. 2004). In Western populations, BE may be present in approximately 0.4–1.6% of adults, whereas in patients with chronic GERD, the prevalence is approximately 10–15% (Pondugula et al. 2007; Wani and Sharma 2007a). The frequency of EAC in the United States is gradually rising. It has been estimated that 14,550 new cases of esophageal cancer were diagnosed in 2006, with 13,770 deaths related to esophageal cancer, the majority diagnosed at an advanced stage (American Cancer Society 2006). Barrett's esophagus is considered to be one of the most important identifiable risk factors leading to development of EAC (Menke-Pluymers et al. 1993; Solaymani-Dodaran et al. 2004). Progression of BE to esophageal cancer involves a series of pathological changes, from early nondysplastic columnar epithelium (ND BE) to low-grade dysplasia (LGD), high-grade dysplasia (HGD), and finally to cancer. The mortality associated with EAC is high, with a 5-year survival rate of only 15% (Pondugula et al.2007; Cossentino and Wong 2003; Devesa et al.1998).
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Barrett's esophagus, a metaplastic precursor to esophageal adenocarcinoma, is becoming increasingly prevalent in many populations. Clinical studies suggest acid reflux causes Barrett's esophagus; however, no population-based estimates of risk have been reported, and the role of other health factors in modifying risk is unclear.We conducted a population-based case-control study in Brisbane, Australia. Cases were 167 patients with histologically confirmed Barrett's esophagus diagnosed between February and December 2003. Age-matched and sex-matched controls (n = 261) were randomly selected from a population register. Data on exposure to self-reported symptoms of acid reflux, smoking, obesity, and other factors were collected through self-completed questionnaires followed by telephone interview. Risks of Barrett's esophagus and Barrett's esophagus with dysplasia associated with these exposures were estimated by the odds ratio (OR) and 95% confidence interval (95% CI), both crude and adjusted for other factors.Self-reported weekly episodes of acid reflux were associated with greatly increased risks of Barrett's esophagus (adjusted OR, 29.7; 95% CI, 12.2-72.6) and Barrett's esophagus with dysplasia (OR, 59.7; 95% CI, 18.5-193). Smoking was also associated with risk of Barrett's esophagus. We found evidence of interactions between symptoms of acid reflux and smoking and obesity. Obese people with self-reported symptoms of acid reflux had markedly higher risks of Barrett's esophagus (OR, 34.4; 95% CI, 6.3-188) than people with reflux alone (OR, 9.3; 95% CI, 1.4-62.2) or obesity alone (OR, 0.7; 95% CI, 0.2-2.4). Similarly, those reporting both acid reflux symptoms and smoking were at substantially higher risks of Barrett's esophagus (OR, 51.4; 95% CI, 14.1-188) than those reporting acid reflux or smoking alone.Although history of symptoms of acid reflux is the principle factor associated with Barrett's esophagus, risks are substantially increased by obesity and smoking.
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Universal agreement on the inclusion of intestinal metaplasia to diagnose Barrett's esophagus (BE) is lacking. Our aim was to determine the association of intestinal metaplasia and its density with the prevalence of dysplasia/cancer in columnar lined esophagus (CLE). Patients with CLE but no intestinal metaplasia (CLE-no IM) were identified by querying the clinical pathology database using SNOMED codes for distal esophageal biopsies. CLE-IM patients were identified from a prospectively maintained database of BE patients. Subsequently, relative risks for prevalent dysplasia and cancer were calculated. Since patients with CLE-no IM are not usually enrolled in surveillance, only prevalent dysplasia/cancer on index endoscopy was analyzed. Goblet cell density and percent intestinal metaplasia were estimated. All biopsy slides were reviewed for dysplasia by two experienced gastrointestinal pathologists. Two hundred sixty-two CLE-IM and 260 CLE-no IM patients were included (age 64 ± 12 vs. 60 ± 11 years, P = 0.001; whites 92% vs. 82%, P = 0.001; males 99.7% vs. 99.3%, P = NS; CLE length 3.4 ± 3.2 vears 1.4 ± 0.4 cm, P = 0.001 and hiatus hernia 64% vs. 56%, P = 0.013). The odds of finding low-grade dysplasia and of high-grade dysplasia (HGD)/cancer were 12.5-fold (2.9–53.8, P = 0.007) and 4.2-fold (95% CI 1.4–13, P = 0.01) higher, respectively, in the CLE-IM group. Reanalysis after controlling for important variables of age, race, and length did not significantly alter the overall results. In CLE-IM group, when patients with high (>50/LPF) versus low goblet cell density (<50/LPF) and <10% versus >10% intestinal metaplasia were compared, the odds of HGD/cancer, OR 1.5 (0.5–4.9, P = 0.5) and 1.97 (0.54–7.22), respectively, were not significantly higher. Demonstration of intestinal metaplasia continues to be an essential element in the definition of BE, but its quantification may not be useful for risk stratification of HGD/cancer in BE.
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Barrett's esophagus has been associated with adenocarcinoma of the esophagogastric junction and gastric cardia. The purpose of this study was to determine whether patients with Barrett's esophagus have a higher prevalence of intestinal metaplasia involving the gastric cardia than those without Barrett's esophagus.Two groups of patients were compared for the prevalence of intestinal metaplasia of the gastric cardia. Group 1 included 50 patients with well-defined Barrett's esophagus who were being followed in an endoscopic surveillance program. Group 2 consisted of 104 individuals participating in a separate study identifying the prevalence of cardia intestinal metaplasia in patients undergoing elective upper endoscopy. Both groups had biopsy specimens taken from the gastric cardia. Eleven patients in group 2 were found to have Barrett's esophagus and were excluded from the analysis. Histological evidence of intestinal metaplasia was defined as specialized columnar epithelium containing goblet cells staining with Alcian blue at pH 2.5.The prevalence of cardia intestinal metaplasia in the 50 patients in group 1 (Barrett's esophagus) was 22%, whereas the prevalence in the 93 patients in group 2 (no Barrett's esophagus) was 24%, which was not a statistically significant difference. A significant difference between groups still could not be identified when the results were examined with regard to equal number of biopsy specimens taken. None of the patients in either group had dysplasia identified within the cardia intestinal metaplasia.Patients with Barrett's esophagus do not have a higher prevalence of intestinal metaplasia of the gastric cardia than those presenting for routine endoscopy. Although intestinal metaplasia of the gastric cardia is a relatively common finding, dysplasia is uncommon. Therefore, we suggest that screening biopsy specimens of the gastric cardia in patients with Barrett's esophagus be limited to study protocols at this time. In addition, we believe that these data raise the question of whether a true association exists between Barrett's esophagus and gastric cardia cancer.
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Barrett's esophagus
Intestinal metaplasia
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Objective To investigate the similarities and differences of endoscopic and pathological char- acteristics between long and short segment Barrett's esophagus.Methods One hundred and twenty-eight cases of Barrett's esophagus identified both by endoscopy and pathology were enrolled in this retrospective study. Among them,40 cases were long segment Barrett's esophagus (LSBE) and 88 were short segment Barrett's esophagus (SSBE).The age distribution,sex distinction,endoscopic manifestations and pathological changes were assessed.Data were statistically analyzed by t-test or u-test.Results There were no differences in age distribution and sex distinction between LSBE and SSBE groups (P＞0.05).The ring pattern was the most prominent type accounting for 62.5% in LSBE group.The island pattern was the most prominent type accounting for 85.2% in SSBE group.There were significant differences in the rates of specialized intestinal metaplasia between LSBE and SSBE groups(47.5% vs 14.8%,P＜0.01).Moreover,among the special- ized intestinal metaplasia,low grade (15.0% vs 4.5%),medium grade (12.5% vs 3.4%) and high grade dysplasia (5.0% vs 0.0%) between LSBE and SSBE groups also had statistical differences (all P＜0.05).Conclusions LSBE may have more tendency in dysplasia than that of SSBE.We should pay attention to the importance of endoscopic manifestations and pathological diagnosis.
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