Between Barrett's Esophagus Research Articles

Association of Barrett's esophagus with obstructive sleep apnea syndrome: a bidirectional analysis of Mendelian randomization.

Observational studies have reported associations between Barrett's esophagus (BE) and obstructive sleep apnea syndrome (OSAS), but the causal relationship remained unclear due to potential confounding biases. Our study aimed to elucidate this causal relationship by deploying a two-sample Mendelian randomization (MR) methodology. Instrumental variables (IVs) for Barrett's esophagus were obtained from a public database that comprised 13,358 cases and 43,071 controls. To investigate OSAS, we utilized summary statistics from a comprehensive genome-wide association study (GWAS) encompassing 38,998 cases of OSAS and 336,659 controls. Our MR analyses adopted multiple techniques, including inverse variance weighted (IVW), weighted median, weighted mode, MR-Egger, and simple mode. The IVW analysis established a causal relationship between Barrett's esophagus and OSAS, with an odds ratio (OR) of 1.19 and a 95% confidence interval (CI) of 1.11-1.28 (p = 8.88E-07). Furthermore, OSAS was identified as a contributing factor to the onset of Barrett's esophagus, with an OR of 1.44 and a 95% CI of 1.33-1.57 (p = 7.74E-19). Notably, the MR-Egger intercept test found no evidence of directional pleiotropy (p > 0.05). This study identifies a potential association between BE and an increased occurrence of OSAS, as well as the reverse relationship. These insights could influence future screening protocols and prevention strategies for both conditions.

Association between coffee or tea drinking and Barrett's esophagus or esophagitis: an Italian study.

Only a few papers have treated of the relationship between Barrett's esophagus (BE) or erosive esophagitis (E) and coffee or tea intake. We evaluated the role of these beverages in BE and E occurrence. Patients with BE (339), E (462) and controls (619) were recruited. Data on coffee and tea and other individual characteristics were collected using a structured questionnaire. BE risk was higher in former coffee drinkers, irrespective of levels of exposure (cup per day; ⩽1: OR=3.76, 95% CI 1.33-10.6; >1: OR=3.79, 95% CI 1.31-11.0; test for linear trend (TLT) P=0.006) and was higher with duration (>30 years: OR=4.18, 95% CI 1.43-12.3; TLT P=0.004) and for late quitters, respectively (⩽3 years from cessation: OR=5.95, 95% CI 2.19-16.2; TLT P<0.001). The risk of BE was also higher in subjects who started drinking coffee later (age >18 years: OR=6.10, 95% CI 2.15-17.3). No association was found in current drinkers, but for an increased risk of E in light drinkers (<1 cup per day OR =1.85, 95% CI 1.00-3.43).A discernible risk reduction of E (about 20%, not significant) and BE (about 30%, P<0.05) was observed in tea drinkers. Our data were suggestive of a reduced risk of BE and E with tea intake. An adverse effect of coffee was found among BE patients who had stopped drinking coffee. Coffee or tea intakes could be indicative of other lifestyle habits with protective or adverse impact on esophageal mucosa.

Metabolic Syndrome as a Risk Factor for Barrett Esophagus: A Population-Based Case-Control Study

ObjectivesTo assess the association between Barrett esophagus (BE) and the metabolic syndrome in patients with and without reflux symptoms and to determine whether this association is reflux independent and metabolically driven. Patients and MethodsCase patients with BE and controls were residents of Olmsted County, Minnesota (1999-2006). Two control groups (one with and one without symptoms of gastroesophageal reflux) were identified from a cohort of patients who had responded to a validated gastrointestinal symptom questionnaire. Cases and controls were individually matched by age, sex, and duration of follow-up. Controls did not have a known diagnosis of BE. The association of the metabolic syndrome and its individual components with BE was assessed using univariate and multivariate conditional logistic regression separately for each control group. ResultsA total of 309 patients were included (103 BE cases, 103 controls with reflux symptoms, and 103 controls without reflux symptoms). A total of 64% of cases, 47% of controls with reflux symptoms, and 50% of controls without reflux symptoms had the metabolic syndrome. The metabolic syndrome was associated with a 2-fold increased risk of BE relative to those with (odds ratio, 2.00; 95% CI, 1.10-3.65; P=.02) and without (odds ratio, 1.90; 95% CI, 1.03-3.60; P=.04) reflux symptoms. This association was independent of smoking, alcohol consumption, and body mass index and remained robust with sensitivity analysis. ConclusionThe metabolic syndrome is associated with BE independent of reflux symptoms, which may reflect a reflux-independent pathway of BE pathogenesis.

Relationship Between Barrett's Esophagus (BE) Length and the Risk of High Grade Dysplasia (HGD) and Esophageal Adenocarcinoma (EAC) in Patients With Non Dysplastic Barrett's Esophagus Results From a Large Multicenter Cohort

Relationship Between Barrett's Esophagus (BE) Length and the Risk of High Grade Dysplasia (HGD) and Esophageal Adenocarcinoma (EAC) in Patients With Non Dysplastic Barrett's Esophagus Results From a Large Multicenter Cohort

Risk of Colorectal Cancer in Patients With Barrett's Esophagus: A Dutch Population-Based Study

The association between Barrett's esophagus (BE) and colorectal cancer (CRC) is controversial. Population-based studies on the risk of CRC in BE are scarce. The aim of this study was to determine the risk of CRC in a nationwide cohort of patients with BE in the Netherlands with long-term follow-up. Patients diagnosed with BE between 1991 and 2006 were identified in the Dutch nationwide histopathology registry (Pathologisch Anatomisch Landelijk Geautomatiseerd Archief (PALGA)). The incidence of CRC observed in these patients was compared with that in the general Dutch population aged >40 years. Relative risks (RRs) and 95% confidence intervals (95% CIs) were calculated using a Poisson model. A total of 42,207 patients with a first diagnosis of BE were included in this study. During a mean follow-up of 5.6 years (s.d. 4), 713 patients (1.7%) were diagnosed with CRC (overall rate: 3.4/1,000 person-years at risk), at a mean age of 73.7 years (s.d. 10). All CRCs occurred in BE patients aged >40 years, and the majority (96%) in those over 50 years of age. Of those CRCs, 317 (44%) were detected within the first year after initial BE diagnosis, and 396 (54%) thereafter. For all patients with BE, CRC risk was 1.70 (95% CI: 1.58-1.83), as compared with the general Dutch population aged >40 years. However, CRC risk within the first year of follow-up after BE diagnosis (RR: 4.76 (95% CI: 4.26-5.31)) was significantly higher than within 1-5 years of follow-up (RR: 0.99 (95% CI: 0.86-1.14)) or more than 5 years of follow-up (RR: 1.28 (95% CI: 1.11-1.47)) (P<0.001). This population-based study shows an overall increased risk of CRC in patients with BE as compared with the general Dutch population, which can for the greater part be explained by diagnostic bias. The magnitude of the association between BE and CRC does not merit a more extensive CRC screening strategy in BE patients than has currently been recommended for the general population.

Abnormal expression of bcl-2 gene family in development of Barrett＇ s esophagus

Objective To detect the differential expression genes （DEGs） between Barrett＇s esophagus （BE） and normal esophagus with oligomicroarray, and to explore the target genes related to the development of BE. Methods The total RNAs of matched BE and normal esophagus mucosa from same patient were isolated with one step Trizol method. Matched RNAs were qualified with 10g/L agarose gel electrophorests. After tRNA purification, cRNAs were synthesized and labeled with fluorescence, which were then hybridized with Agilent oligomicroarray containing 30,968 probes. The fluorescence intensity features were detected by Agilent scanner and quantified by software Feature Extraction. Results On average, 2 biopsies by disposable jumbo biopsy forceps provided approximately 5 μg RNA required for microarray. The total RNA, reverse transcription product and fluorescence labeled cRNA were all of high quality. Among 2-fold DEGs, there were 142 up-regulated genes and 284 down-regulated genes including 15 bcl-2 related genes such as bcl-2, MCL1, BAX, BIK and BCLAF1. Conclusion Microarray-based studies are feasible in endoscopieally obtained tissues. The development of BE is a complicated process involving multi-genes, in which abnormal expression of bcl-2 family related genes might be involved, but the exact mechanism needs further research. Key words: Barrett esophagus; Genes, bcl-2 ; Gene differential expression profile

Oligomicroarray-based primary study of gene expression profile changes in Barrett's esophagus

Objective To analyze the differential expression genes (DEGs) between Barrett's esophagus (BE) and normal esophagus mucosa and explore the target genes related to the development and progression of BE. Methods The total RNAs of matched BE and normal esophagus mucosa of BE patients were isolated using one step Trizol method. Matched RNAs were qualified using 10 g/L agarose gel electrophoresis. cRNAs were synthesized, fluorescence labeled and purified after total RNAs were purified. The RNAs of BE and normal esophagus mucosa were hybridized with Agilent oligomicroarray (30 968 probes). The fluorescence intensity features were detected by Agilent scanner and quantified by feature extraction software. Results (1) The total RNA, reverse transcription product and fluorescence labeled cRNA were all of high quality; (2) There were 142 up-regulated genes and 284 down-regulated genes among 2-fold DEGs. Conclusion Microarray-based studies are feasible in endoscopically obtained tissues. Many BE-associated genes are screened by the high-throughput gene chip. The development and progression of BE is a complicated process involving multiple genes and multiple procedures, and functional study of these genes may help to identify the key genes or pathways involved in the pathogenesis and development of BE.

The Association Between Obesity and GERD: A Review of the Epidemiological Evidence

The current epidemics of obesity and gastroesophageal reflux disease (GERD)-related disorders have generated much interest in studying the association between them. Results of multiple studies indicate that obesity satisfies several criteria for a causal association with GERD and some of its complications, including a generally consistent association with GERD symptoms, erosive esophagitis, and esophageal adenocarcinoma. An increase in GERD symptoms has been shown to occur in individuals who gain weight but continue to have a body mass index (BMI) in the normal range, contributing to the epidemiological evidence for a possible dose-response relationship between BMI and increasing GERD. Data are less clear on the relationship between Barrett's esophagus (BE) and obesity. However, when considered separately, abdominal obesity seems to explain a considerable part of the association with GERD, including BE. Overall, epidemiological data show that maintaining a normal BMI may reduce the likelihood of developing GERD and its potential complications.

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis

To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.

Colorectal Neoplasia in Veterans Is Associated with Barrett's Esophagus but Not with Use of Proton-Pump Inhibitors (PPIs) or Aspirin/NSAIDs

Purpose: An association between Barrett's esophagus (BE) and colorectal neoplasia has been suggested, but is still controversial. We investigated whether BE was associated with an increased risk of colorectal neoplasia, and, if so, whether BE was an independent risk factor or dependent on the use of PPIs or aspirin/NSAIDs. Methods: We performed a case-control study and matched 268 veterans with histologically-proven BE (mean length: 2.0 cm, range: 0.5-10 cm, all intestinal metaplasia) with 268 controls without BE. Controls had undergone upper GI endoscopy close (+/- 14 days) to the time of the corresponding case. Colonoscopy was performed within 6 months of the upper GI endoscopy. Charts were reviewed and scored for patient characteristics (age, gender, ethnicity, and body mass index (BMI)), tobacco or alcohol use, and use of PPIs and aspirin/NSAIDs for at least 6 months prior to upper GI endoscopy, and findings at colonoscopy. Statistical analysis was done by t-tests, chi-square tests and logistic regression analysis. Results: Mean age was 66 +/- 11 years in the BE group and 64 +/- 12 years in the control group. The majority were men (BE group 99% vs. controls: 97%) and white (74% vs. 72%). Mean BMI was similar (28 +/- 6 vs. 29 +/- 6) as was smoking (40% vs. 34%), but alcohol use was more common in the BE group (66% vs. 46%, p < 0.001). BE patients used more often PPIs (54% vs. 25% (p < 0.001), but less often aspirin/NSAIDs (50% vs. 61%, p=0.007). Colorectal adenomas or carcinoma were present in 160 /268 (60%) patients of the BE group and in 105/268 (39%) controls (p<0.001). The total number of polyps (BE group vs. controls: 1.8 vs 1.9) and the mean size of the polyps (0.60 vs. 0.55 mm) were similar in those with polyps. Increasing age (OR 1.23 per decade, 95% CI (1.02, 1.49)), use of alcohol (OR 1.76: 95% CI (1.19, 2.60)), and BE (OR 1.93: 95% CI (1.29, 2.91)) were associated with an increased risk of developing colorectal neoplasia, when statistically adjusted for each other and other potential risk factors in multivariate analysis. Conclusion: These results suggest that veterans with BE are at an increased risk of developing colorectal neoplasia. This association is independent from the use of PPIs or aspirin/NSAIDs.

Characteristics of acid reflux in Barrett's esophagus.

To determine the relationship between Barrett's esophagus (BE) and features of gastroesophageal acid reflux, 24 h esophageal pH monitoring was performed in 90 patients. The patients were divided into 3 groups: 31 subjects with BE, 21 with mild esophagitis and 38 with severe esophagitis. The following parameters were evaluated: the percentage time of pH < 4; the number of reflux episodes over 5 min; the duration of longest episodes and DeMeester score over total period and the auterior three parameters in erect and supine position. All these parameters in BE were significantly different from those with mild esophagitis (P < 0.01) and not significantly different from those with severe esophagitis (P > 0.05). During supine position all the above parameters in BE were significantly different from those with reflux esophagitis (P < 0.05). It is concluded that the quantity of acid reflux is not an important factor in development of BE in gastroesophageal reflux (GER), and the acid reflux in supine position might be important in development of BE in GER.