Lifestyle interventions can reduce the risk of Barrett's esophagus: a systematic review and meta-analysis of 62 studies involving 250,157 participants.

BACKGROUND: Barrett's esophagus (BE) is a well-established risk factor for esophageal adenocarcinoma. Our objective was to investigate the effectiveness of lifestyle interventions on BE risk. METHODS: We searched PubMed, Embase, and Web of Science up to 30 September 2020. The summary relative risks (RRs) and 95% confidence intervals (CIs) for the highest versus lowest categories of exposure were assessed. Analyses of subgroup, dose-response, sensitivity, and publication bias were conducted. RESULTS: Sixty-two studies were included that involved more than 250,157 participants and 22,608 cases. Seven lifestyle factors were investigated: smoking, alcohol, body mass index (BMI), physical activity, sleep time, medication, and diet. We observed statistically significant increased BE risks for smoking (RR = 1.35, 95% CI = 1.16-1.57), alcohol intake (RR = 1.23, 95% CI = 1.13-1.34), body fatness (RR = 1.08, 95% CI = 1.03-1.13), less sleep time (RR = 1.76, 95% CI = 1.24-2.49), and proton pump inhibitors use (RR = 1.64, 95% CI = 1.17-2.29). Reduced risks of BE were found for aspirin (RR = 0.70, 95% CI = 0.58-0.84) and the intake of vitamin C (RR = 0.59, 95% CI = 0.44-0.80), folate (RR = 0.47, 95% CI = 0.31-0.71), and fiber (RR = 0.95, 95% CI = 0.93-0.97). The quality of most included studies was high and the subgroup analysis according to the quality score showed significant results (p < 0.05). There was no publication bias for smoking and alcohol. Although the analysis suggested significant evidence of publication bias for BMI, sensitivity analysis showed that the changes in the recalculated RRs were not significant. CONCLUSIONS: The large meta-analysis revealed that lifestyle modifications could reduce the risks of BE and, consequently, esophageal adenocarcinoma.

Effect of nonsteroidal anti-inflammatory drugs on Barrett's esophagus risk: a systematic review and meta-analysis.

OBJECTIVE: Conflicting evidence exists regarding the effect of NSAIDs on the risk of Barrett's esophagus. The purpose of this study is to systematically assess this effect through a meta-analysis. METHODS: Accordingly, clinical studies on NSAID use and Barrett's esophagus risk were searched on PubMed, Embase, and the Cochrane Library. Following this, meta-analyses were conducted using the RevMan 5.3 software. The pooled odds ratio (OR) and corresponding 95% confidence interval (CI) were used as the effect size. RESULTS: Seven eligible studies (one cohort study and six case-control studies) were included for the present meta-analysis by adopting a fixed-effect model, which demonstrated that NSAIDs could reduce Barrett's esophagus risk (OR: 0.84, 95%CI:0.75-0.94, P＜0.05). Moreover, subgroup analyses done according to sex showed that NSAIDs could reduce Barrett's esophagus risk in females (OR 0.85; 95% CI 0.73-0.99; P = 0.04), without heterogeneity between studies (P = 1.00 and I2 = 0%). However, this relationship was not evident in males (OR 0.85; 95% CI 0.68-1.07; P = 0.16). CONCLUSIONS: Overall, this meta-analysis provided high quality evidence that use of NSAIDs is associated with a reduced risk of Barrett's esophagus. However, the presence of a sex-dependent difference remains to be clarified.

Laparoscopic Nissen Fundoplication: How I Do It?

Surgical treatment of gastroesophageal reflux disease (GERD) aims to control patients' symptoms, improve patients' quality of life, and prevent GERD-related complications (bleeding, esophageal stenosis, Barrett's esophagus, and/or esophageal adenocarcinoma). A careful patient selection and a properly executed operation are key for the success of the procedure. We aimed to describe the operative technique of a laparoscopic Nissen fundoplication, stressing the critical surgical steps we believe should be respected to obtain good surgical outcomes.

Erosive Esophagitis Portends a Benign Clinical Course in the Majority of Patients.

INTRODUCTION: Indefinite proton pump inhibitor (PPI) therapy and endoscopic evaluation for Barrett's esophagus is recommended for erosive esophagitis (EE). However, the clinical course of EE remains undefined. METHODS: Adults with EE on esophagogastroduodenoscopy (EGD) were identified at Mayo Clinic Rochester between January 2003 and September 2005. Patients with repeat EGD performed after index endoscopy were included. Patients with a history of upper gastrointestinal surgery, esophageal cancer, achalasia, or Barrett's on initial EGD were excluded. RESULTS: Of 219 patients identified, 98 had LA grade A, 72 LA grade B, and 49 LA grade C esophagitis. Persistent EE was found in 27% on repeat endoscopy. No patients progressed to more severe grades of esophagitis. While discontinuation of PPI was associated with persistent esophagitis, long-term healing of esophagitis occurred in the majority of patients despite discontinuation of PPI. Grade A or B esophagitis and the absence of hiatal hernia were also independent predictors of esophagitis healing on multivariate analysis. The rate of Barrett's esophagus was similar among patients with LA grade A/B and C esophagitis on initial EGD (5% vs. 14%, p = 0.6). CONCLUSION: The majority of patients with EE demonstrated healing at follow-up endoscopy regardless of continued PPI use. A small proportion developed Barrett's esophagus, including those with LA grade A and B esophagitis, highlighting a potential role for repeat endoscopy in all grades of EE. A more conservative long-term PPI strategy may be reasonable in patients with LA grade A or B esophagitis in the absence of hiatal hernia.

No Barrett's-No Cancer: A Proposed New Paradigm for Prevention of Esophageal Adenocarcinoma.

Esophageal adenocarcinoma is inflammation-associated cancer with a recognizable preneoplastic stage, Barrett's. Barrett's describes the metaplastic transformation of esophageal squamous mucosa into columnar epithelium that typically results secondary to mucosal damage caused by acidic gastroduodenal reflux. Continued acid reflux may then result in mucosal inflammation which results in progressive inflammation-induced genetic instability that may eventuate in esophageal adenocarcinoma. Barrett's is the only recognized precursor lesion to esophageal carcinoma. Barrett's mucosa is unique among preneoplastic lesions; ablation therapy results in restitution of a squamous epithelium reducing or eliminating accumulated genetic instabilities and resetting the biological clock progressing toward invasive cancer. However, recurrence of Barrett's after ablation is common. We propose that both Barrett's and recurrence of Barrett's after ablation can be prevented and discuss how current approaches to therapy for gastroesophageal reflux disease, for Barrett's screening, chemoprevention, and ablation therapy all might be reconsidered. We propose (1) improved approaches to Barrett's prevention, (2) universal Barrett's screening by linking Barrett's screening to colon cancer screening, (3) ablation of all Barrett's mucosa along with (4) acid-suppressive-antireflux therapy tailored to prevent development of Barrett's or the recurrence of Barrett's after ablation therapy. We propose that ultimately, treatment decisions for gastroesophageal reflux disease and prevention of Barrett's and esophageal carcinoma should be based on assessing and maintaining esophageal mucosal integrity. This will require development and verification of specific measurements that reliably correlate with prevention of Barrett's. We outline the new research and technical advances needed to cost-effectively achieve these goals.

Pathology, Chemoprevention, and Preclinical Models for Target Validation in Barrett Esophagus.

Despite esophageal adenocarcinoma (EAC) being the most widespread among gastrointestinal cancers, with an 11-fold increase in the risk of cancer for patients with Barrett esophagus (BE), its prognosis is still poor. There is a critical need to better perceive the biology of cancer progression and identification of specific targets that are the hallmark of BE's progression. This review explores the established animal models of BE, including genetic, surgical and nonsurgical approaches, potential chemoprevention targets, and the reasoning behind their applications to prevent Barrett-related EAC. The key methodological features in the design feasibility of relevant studies are also discussed. Cancer Res; 78(14); 3747-54. ©2018 AACR.

Melatonin in Prevention of the Sequence from Reflux Esophagitis to Barrett's Esophagus and Esophageal Adenocarcinoma: Experimental and Clinical Perspectives.

Melatonin is a tryptophan-derived molecule with pleiotropic activities which is produced in all living organisms. This "sleep" hormone is a free radical scavenger, which activates several anti-oxidative enzymes and mechanisms. Melatonin, a highly lipophilic hormone, can reach body target cells rapidly, acting as the circadian signal to alter numerous physiological functions in the body. This indoleamine can protect the organs against a variety of damaging agents via multiple signaling. This review focused on the role played by melatonin in the mechanism of esophagoprotection, starting with its short-term protection against acute reflux esophagitis and then investigating the long-term prevention of chronic inflammation that leads to gastroesophageal reflux disease (GERD) and Barrett's esophagus. Since both of these condition are also identified as major risk factors for esophageal carcinoma, we provide some experimental and clinical evidence that supplementation therapy with melatonin could be useful in esophageal injury by protecting various animal models and patients with GERD from erosions, Barrett's esophagus and neoplasia. The physiological aspects of the synthesis and release of this indoleamine in the gut, including its release into portal circulation and liver uptake is examined. The beneficial influence of melatonin in preventing esophageal injury from acid-pepsin and acid-pepsin-bile exposure in animals as well as the usefulness of melatonin and its precursor, L-tryptophan in prophylactic and supplementary therapy against esophageal disorders in humans, are also discussed.

The Influence of Antireflux Surgery on Esophageal Cancer Risk in England: National Population-based Cohort Study.

OBJECTIVE: To evaluate how antireflux surgery influences the risk of esophageal cancer in patients with gastroesophageal reflux disease (GERD) and Barrett esophagus. BACKGROUND: GERD is a major risk factor for esophageal adenocarcinoma, and the United Kingdom has the highest incidence of esophageal adenocarcinoma globally. METHODS: Hospital Episode Statistics database was used to identify all patients in England aged over 18 years diagnosed with GERD with or without Barrett Esophagus from 2000 to 2012, with antireflux surgery being the exposure investigated. The Clinical Practice Research Datalink (CPRD) was used to provide a sensitivity analysis comparing proton pump inhibitor therapy and antireflux surgery. Hazard ratios (HR) with 95% confidence intervals (CI) were calculated using Cox proportional hazards model with inverse probability weights based on the probability of having surgery to adjust for selection bias and confounding factors. RESULTS: (i) Hospital Episode Statistics analysis; among 838,755 included patients with GERD and 28,372 with Barrett esophagus, 22,231 and 737 underwent antireflux surgery, respectively. In GERD patients, antireflux surgery reduced the risk of esophageal cancer (HR = 0.64; 95% CI 0.52-0.78). In Barrett esophagus patients, the corresponding HR was (HR = 0.47; 95% CI 0.12-1.90).(ii) CPRD analysis; antireflux surgery was associated with decreased point estimates of esophageal adenocarcinoma in patients with GERD (0% vs. 0.2%; P = 0.16) and Barrett esophagus (HR = 0.75; 95% CI 0.21-2.63), but these were not statistically significant. CONCLUSION: Antireflux surgery may be associated with a reduced risk of esophageal cancer risk, however it remains primarily an operation for symptomatic relief.

Aspirin: the miracle drug?

Aspirin use is associated with reduction of esophageal adenocarcinoma but it is not known if it does so by preventing the development of Barrett's esophagus or by reducing neoplastic progression in patients with Barrett's esophagus. There is sparse literature to support the former assumption especially in women. This study by Jovani et al. based on Nurses' Health Study reports 27% lower risk of Barrett's esophagus among women using aspirin. The protective effect seems to increase with higher frequency and longer duration of aspirin use. This study provides evidence for lower prevalence of Barrett's esophagus in female aspirin users.

The association between physical activity and the risk of symptomatic Barrett's oesophagus: a UK prospective cohort study.

BACKGROUND: Physical activity affects the functioning of the gastrointestinal system through both local and systemic effects and may play an important role in the aetiology of gastroesophageal reflux disease, Barrett's oesophagus and oesophageal adenocarcinoma. We investigated, for the first time in a large prospective cohort study, associations between recreational and occupational levels of physical activity and the incidence of Barrett's oesophagus. PARTICIPANTS AND METHODS: The European Prospective Investigation of Cancer-Norfolk recruited 30 445 men and women between 1993 and 1997. Occupational and recreational levels of physical activity were measured using a baseline questionnaire. The cohort was followed up until 2015 to identify symptomatic cases of Barrett's oesophagus. Cox proportional hazard regression estimated hazard ratios (HR) for physical activity and the development of disease. RESULTS: Two hundred and three participants developed Barrett's oesophagus (mean age: 70.6 years) the majority of whom were men (70.9%). There was an inverse association between standing occupations and disease risk [HR: 0.50, 95% confidence interval (CI): 0.31-0.82, P=0.006] when compared with sedentary jobs. Heavy manual occupations were positively associated with disease risk (HR: 1.66, 95% CI: 0.91-3.00), but conventional statistical significance was not reached (P=0.09). No associations were found between recreational activity and the risk of Barrett's oesophagus (HR: 1.34, 95% CI: 0.72-2.50, P=0.35, highest vs. lowest levels of activity). CONCLUSION: Our study suggests that occupational levels of physical activity may be associated with the risk Barrett's oesophagus. However, further work is required to confirm and describe specific occupations that may be protective.

Proceedings from an international conference on ablation therapy for Barrett's mucosa: Brittany, France, 31 August - 2 September 1997.

The increasing incidence of adenocarcinoma of the lower esophagus and cardia arising in Barrett's metaplastic epithelium continues to be of great concern because medical and surgical efforts to reverse the process have been disappointing. A potential answer to the problem is removal of the metaplastic epithelium. Modern technology has introduced physical and chemical modalities which facilitate ablation of the neo-epithelium endoscopically. These techniques have been used in several centers, and preliminary results are encouraging. This report summarizes the proceedings of an international symposium on ablative therapy held in Brittany, France in August 1997.Twenty-eight speakers contributed to the talks on the pathology, pathogenesis, current therapy experimental studies and clinical experience of ablation of Barrett's esophagus.

Does physical activity protect against the development of gastroesophageal reflux disease, Barrett's esophagus, and esophageal adenocarcinoma? A review of the literature with a meta-analysis.

Physical activity affects the functioning of the gastrointestinal system through both local and systemic effects and may play an important role in reducing the risk of esophageal adenocarcinoma. This review assesses the biological mechanisms and epidemiological evidence for the relationship between physical activity and the development of esophageal adenocarcinoma and its precursor diseases: gastroesophageal reflux disease (GORD) and Barrett's esophagus. A search of PubMed, Medline, Embase, and CINAHL was conducted from their inceptions to 25th March 2017 for analytical studies that examined associations between recreational and/or occupational levels of physical activity and the risk of GORD, Barrett's esophagus, and esophageal adenocarcinoma. Where appropriate, a meta-analysis of effects was undertaken. Seven studies were included (2 cohort, 5 case control). For GORD, there were three case-control studies with 10 200 cases among 78 034 participants, with a pooled estimated OR of 0.67 (95% CI 0.57-0.78) for high versus low levels of recreational physical activity. In Barrett's esophagus, there was a single case-control study, which reported no association, OR 1.19 (95% CI 0.82-1.73). For esophageal adenocarcinoma, there were three studies (two prospective cohort, one case control) with 666 cases among 910 376 participants. The largest cohort study reported an inverse association for high versus low levels of recreational physical activity, RR 0.68, 95% CI 0.48-0.96. The remaining two studies reported no associations with either occupational or combined recreational and occupational activity. Heterogeneity in the measurement of exposure (recreational, occupational, and both) made a pooled estimate for esophageal adenocarcinoma inappropriate. Although limited, there is some evidence that higher levels of recreational physical activity may reduce the risk of both GORD and esophageal adenocarcinoma, but further large cohort studies examining the type, intensity and duration of activities that may be beneficial are needed.

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

BACKGROUND/OBJECTIVES: 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. SUBJECTS/METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Recurrence of Barrett's Esophagus is Rare Following Endoscopic Eradication Therapy Coupled With Effective Reflux Control.

OBJECTIVES: Recent data suggest that effective control of gastroesophageal reflux improves outcomes associated with endoscopic eradication therapy (EET) for Barrett's esophagus (BE). However, the impact of reflux control on preventing recurrent intestinal metaplasia and/or dysplasia is unclear. The aims of the study were: (a) to determine the effectiveness and durability of EET under a structured reflux management protocol and (b) to determine the impact of optimizing anti-reflux therapy on achieving complete eradication of intestinal metaplasia (CE-IM). METHODS: Consecutive BE patients referred for EET were enrolled and managed with a standardized reflux management protocol including twice-daily PPI therapy during eradication. Primary outcomes were rates of CE-IM and IM or dysplasia recurrence. RESULTS: Out of 221 patients enrolled (46.0% with high-grade dysplasia/intramucosal carcinoma, 34.0% with low-grade dysplasia, and 20.0% with non-dysplastic BE) an overall CE-IM of 93% was achieved within 11.6±10.2 months. Forty-eight patients did not achieve CE-IM in 3 sessions. After modification of their reflux management, 45 (93.7%) achieved CE-IM in a mean of 1.1 RFA sessions. Recurrence occurred in 13 patients (IM in 10(4.8%), dysplasia in 3 (1.5%)) during a mean follow-up of 44±18.5 months. The only significant predictor of recurrence was the presence of a hiatal hernia. Recurrence of IM was significantly lower than historical controls (10.9 vs. 4.8%, P=0.04). CONCLUSIONS: The current study highlights the importance of reflux control in patients with BE undergoing EET. In this setting, EET has long-term durability with low recurrence rates providing early evidence for extending endoscopic surveillance intervals after EET.

Displasia de alto grado en esófago de Barrett: ¿ablación, mucosectomía o cirugía? / High-grade dysplasia in Barrett's oesophagus: ablation, mucosectomy or surgery?

Barrett's esophagus has a risk of developing esophageal adenocarcinoma and it increases when dysplasia is present. For this reason, its diagnosis requires endoscopic surveillance or eradication if dysplasia or cancer appears. In the past, high-grade dysplasia and intramucosal esophageal adenocarcinoma were routinely treated with esophagectomy, but with considerable morbidity and mortality. This has led to the development of new alternatives as less invasive endoscopic treatments for both dysplastic lesion and total eradication of the remaining metaplastic mucosa. The most commonly used treatment options include cryotherapy, radiofrequency ablation, endoscopic resection (mucosal resection or endoscopic submucosal dissection) or a combination of these (multimodal endoscopic eradication). For patients with low-grade dysplasia still some international guides suggest keeping endoscopic follow up; however, considering the good results of endoscopic ablation and new evidence about the course of this disease, this concept has changed towards the therapeutic approach. For Barrett´s esophagus without any complication, endoscopic therapy is not recommended, but endoscopic surveillance. In this article we will review the endoscopic therapeutic alternatives to Barrett's esophagus, its scientific basis and how they have evolved in recent times.

El Esófago de Barrett es una lesión adquirida que tiene riesgo de desarrollar adenocarcinoma esofágico. Su presencia obliga, por lo tanto, a la vigilancia endoscópica y erradicación cuando aparece displasia sobre este epitelio, pues aumenta la probabilidad de progresar a cáncer. Antes de la aparición de la terapia endoscópica estos casos con displasia de alto grado y adenocarcinoma esofágico independiente de su estadío, eran sometidos a una esofagectomía. Sin embargo, esta intervención se asocia a una morbimortalidad importante. De esta manera, los avances en la cirugía endoscópica también han sido traspasados al manejo del Esófago de Barrett con displasia o cáncer intramucoso, que incluyen en estos casos la erradicación del epitelio columnar en su totalidad. Las alternativas terapéuticas más utilizadas son la crioterapia, ablación por radiofrecuencia, resección endoscópica (mucosectomía o disección submucosa endoscópica) o una combinación de éstas (erradicación endoscópica multimodal). Para pacientes portadores de Barrett con displasia de bajo grado, la recomendación de la mayoría de las guías internacionales sigue siendo la vigilancia endoscópica. Sin embargo, dado los buenos resultados de la ablación endoscópica y nuevas evidencias respecto al curso de esta patología, este concepto ha ido cambiando hacia tomar una conducta terapéutica. En caso de ausencia de displasia no se recomienda la terapia endoscópica de regla sino la vigilancia endoscópica. En el presente artículo revisaremos las alternativas terapéuticas endoscópicas frente al esófago de Barrett, su sustento científico y cómo han evolucionado en el último tiempo.

Adherence to WCRF/AICR lifestyle recommendations for cancer prevention and the risk of Barrett's esophagus onset and evolution to esophageal adenocarcinoma: results from a pilot study in a high-risk population.

PURPOSE: While adherence to the World Cancer Research Fund (WCRF) guidelines on lifestyle and cancer was recently proven to be associated with an increased risk of esophageal cancer, no investigation has yet been carried out on its role on Barrett's esophagus (BE) development and its progression to esophageal adenocarcinoma (EAC). The primary aim of this study was to evaluate the role of adherence to WCRF lifestyle recommendations in BE onset and progression. The secondary aim was to investigate the association between disease progression and specific aspects of diet and lifestyle. METHODS: Established risk factors for BE and EAC development and adherence to WCRF guidelines were assessed in 107 consecutive patients undergoing an upper gastrointestinal endoscopy for symptoms suggesting gastroesophageal reflux (GERD) and a suspected diagnosis of BE/dysplasia on BE. Patients were divided according to histology: those with GERD without metaplasia, with non-dysplastic BE, with low-grade dysplasia, with high-grade dysplasia or with early EAC. The four groups were expressed as an ordered categorical variable of disease progression. An ordered logit model was estimated to identify the independent predictors of disease progression. RESULTS: Adherence to WCRF guidelines was identified as independent protective factor (OR 0.51, 95 % CI 0.37-0.67) of disease progression. Disease progression was associated with reduced adherence to guidelines on physical activity (from 48.2 to 5.3 %, p = 0.001), sedentary habits (from 33.3 to 0 %, p = 0.03), fruit consumption (from 37.0 to 5.6 %, p = 0.02) and processed meat consumption (from 51.9 to 10.5 %, p = 0.002). CONCLUSION: Adherence to WCRF guidelines has a protective factor in BE onset and its evolution to EAC.

Dietary magnesium, calcium:magnesium ratio and risk of reflux oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma: a population-based case-control study.

Evidence suggests a role of Mg and the ratio of Ca:Mg intakes in the prevention of colonic carcinogenesis. The association between these nutrients and oesophageal adenocarcinoma - a tumour with increasing incidence in developed countries and poor survival rates - has yet to be explored. The aim of this investigation was to explore the association between Mg intake and related nutrients and risk of oesophageal adenocarcinoma and its precursor conditions, Barrett's oesophagus and reflux oesophagitis. This analysis included cases of oesophageal adenocarcinoma (n 218), Barrett's oesophagus (n 212), reflux oesophagitis (n 208) and population-based controls (n 252) recruited between 2002 and 2005 throughout the island of Ireland. All the subjects completed a 101-item FFQ. Unconditional logistic regression analysis was applied to determine odds of disease according to dietary intakes of Mg, Ca and Ca:Mg ratio. After adjustment for potential confounders, individuals consuming the highest amounts of Mg from foods had significant reductions in the odds of reflux oesophagitis (OR 0·31; 95 % CI 0·11, 0·87) and Barrett's oesophagus (OR 0·29; 95 % CI 0·12, 0·71) compared with individuals consuming the lowest amounts of Mg. The protective effect of Mg was more apparent in the context of a low Ca:Mg intake ratio. No significant associations were observed for Mg intake and oesophageal adenocarcinoma risk (OR 0·77; 95 % CI 0·30, 1·99 comparing the highest and the lowest tertiles of consumption). In conclusion, dietary Mg intakes were inversely associated with reflux oesophagitis and Barrett's oesophagus risk in this Irish population.

Reduced Risk of Barrett's Esophagus in Statin Users: Case-Control Study and Meta-Analysis.

BACKGROUND: Use of statins has been associated with a reduced incidence of esophageal adenocarcinoma in population-based studies. However there are few studies examining statin use and the development of Barrett's esophagus. AIM: The purpose of this study was to examine the association between statin use and the presence of Barrett's esophagus in patients having their first gastroscopy. METHODS: We have performed a case-control study comparing statin use between patients with, and without, an incident diagnosis of non-dysplastic Barrett's esophagus. Male Barrett's cases (134) were compared to 268 male age-matched controls in each of two control groups (erosive gastro-esophageal reflux and dyspepsia without significant upper gastrointestinal disease). Risk factor and drug exposure were established using standardised interviews. Logistic regression was used to compare statin exposure and correct for confounding factors. We performed a meta-analysis pooling our results with three other case-control studies. RESULTS: Regular statin use was associated with a significantly lower incidence of Barrett's esophagus compared to the combined control groups [adjusted OR 0.62 (95 % confidence intervals 0.37-0.93)]. This effect was more marked in combined statin plus aspirin users [adjusted OR 0.43 (95 % CI 0.21-0.89)]. The inverse association between statin or statin plus aspirin use and risk of Barrett's was significantly greater with longer duration of use. Meta-analysis of pooled data (1098 Barrett's, 2085 controls) showed that statin use was significantly associated with a reduced risk of Barrett's esophagus [pooled adjusted OR 0.63 (95 % CI 0.51-0.77)]. CONCLUSIONS: Statin use is associated with a reduced incidence of a new diagnosis of Barrett's esophagus.