A study to determine plasma antioxidant concentrations in patients with Barrett’s oesophagus

Clements, Debbie; Oleesky, D A; Smith, S C; Wheatley, H; Hullin, David A.; Havard, Timothy; Bowrey, David J.

doi:10.1136/jcp.2004.023721

Cited by 11 publications

(10 citation statements)

References 24 publications

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“…On the other hand, the FINBAR study did not find a significant association between antioxidants and risk of BE [4]. In a molecular epidemiologic study of 36 patients with BE, 32 patients with erosive esophagitis, and 35 patient controls, patients with BE had significantly lower plasma concentrations of selenium, vitamin C, β cryptoxanthin, and lutein/xanthophyll compared with the other groups [17]. Therefore, the data are conflicting on the role of antioxidants in BE development, with more evidence suggesting a protective role of vitamin C, E, and lutein.…”

Section: Discussionmentioning

confidence: 99%

Dietary intake of vegetables, folate, and antioxidants and the risk of Barrett’s esophagus

Jiao

Kramer

Rugge

et al. 2013

Cancer Causes Control

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Purpose Diet is a potentially modifiable risk factor for Barrett's esophagus (BE). We investigated the associations between intakes of fruits and vegetables and risk of BE. Methods We identified study subjects from 1,859 participants who underwent the endoscopy in a single VA Medical Center in the U.S between 2008 and 2011. Dietary intake in the previous year was elicited using a self-administered Block food frequency questionnaire (FFQ). Logistic regression model was used to estimate odds ratio (OR) and its 95% confidence interval (CI) for BE. Results A total of 151 cases with definite BE and 777 controls completed the FFQ. When highest tertile of intake was compared with the lowest, the OR (95% CI) was 0.46 (0.26-0.81) for dark green vegetables, 0.52 (0.30- 0.90) for legumes, 0.50 (0.28-0.90) for total fiber, 0.45 (0.25-0.81) for isoflavones, 0.52 (0.30- 0.67) for total folate, and 0.45 (0.26-0.79) for lutein, adjusting for multiple confounding factors including use of aspirin or proton pump inhibitor, gastro-esophageal reflux symptoms, and physical activity. The association for dark green vegetables was attenuated after adjustment for lutein, total fiber, and total folate (OR = 0.82; 95% CI, 0.30-2.22). Conclusion Higher intake of dark green vegetables was associated with a decreased risk of BE in a veteran population. Such an inverse association may be partially mediated by lutein, fiber and folate. The novel findings on the association between intake of lutein, total folate, or isoflavones and risk of BE need further confirmation.

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Section: Discussionmentioning

confidence: 99%

Dietary intake of vegetables, folate, and antioxidants and the risk of Barrett’s esophagus

Jiao

Kramer

Rugge

et al. 2013

Cancer Causes Control

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“…A recent study from Ireland reported an inverse association between fruits and vegetables intake and the risk of Barrett’s esophagus,26 and another hospital-based study reported an inverse association between vitamin C intake and Barrett’s esophagus,27 though both study used only population-controls as a comparison group. Another study that examined the plasma concentration of antioxidants and the risk of Barrett’s esophagus reported that Barrett’s esophagus patients had lower levels of plasma antioxidants such as selenium and vitamin C compared to controls 28. However, plasma biomarkers do not provide definitive information on patterns of food consumption (such as fruit and vegetable), and cannot separate dietary vs. supplement intake; these factors are all important in planning potential nutritional interventions 29…”

Section: Introductionmentioning

confidence: 99%

Dietary Antioxidants, Fruits, and Vegetables and the Risk of Barrett's Esophagus

Kubo¹,

Levin²,

Block³

et al. 2008

The American Journal of Gastroenterology

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OBJECTIVE The present study evaluated the associations between antioxidants, fruit and vegetable intakes and the risk of Barrett’s esophagus, a potential precursor to esophageal adenocarcinoma. METHODS We conducted a case-control study within the Kaiser Permanente Northern California population. Incident Barrett’s esophagus cases (n=296) were matched to persons with gastroesophageal reflux disease (GERD) (GERD controls, n=308) and to population controls (n=309). Nutrient intake was measured using a validated 110-item food frequency questionnaire. The antioxidant results were stratified by dietary vs. total intake of antioxidants. RESULTS Comparing cases to population controls, dietary intake of vitamin C and beta-carotene were inversely associated with the risk of Barrett’s esophagus [4th vs. 1st quartile, adjusted odds ratio [OR]=0.48 95% confidence interval [CI] (0.26–0.90); OR=0.56 95%CI(0.32–0.99), respectively], and the inverse association was strongest for vitamin E [OR=0.25 95%CI (0.11–0.59)]. The inverse trends for antioxidant index (total and dietary) and fruit and vegetable intake were statistically significant, while most total intakes were not associated with reduced risk. The use of antioxidant supplements did not influence the risk of Barrett’s esophagus, and antioxidants and fruits and vegetables were inversely associated with a GERD diagnosis. CONCLUSION Dietary antioxidants, fruit and vegetable are inversely associated with the risk of Barrett’s esophagus, while no association was observed for supplement intake. Our results suggest that fruits and vegetables themselves or associated undetected confounders may influence early events in the carcinogenesis of esophageal adenocarcinoma.

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“…GPX3 is a selenium‐containing protein, and this microelement is required for normal functioning of GPX3. It was shown that patients with BE had significantly lower plasma concentrations of selenium, although a population‐based study failed to show that a diet containing selenium has a protective effect against cancer progression in BE patients . Moreover, BE patients with high serum selenium level (upper three quarters) had significantly lower risk of LOH of TP53 .…”

Section: Gpx3 and Nox5 In Be Progressionmentioning

confidence: 99%

Overview of major molecular alterations during progression from Barrett's esophagus to esophageal adenocarcinoma

Kalatskaya

2016

Annals of the New York Academy of Sciences

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Esophageal adenocarcinoma (EAC) develops in the sequential transformation of normal epithelium into metaplastic epithelium, called Barrett's esophagus (BE), then to dysplasia, and finally cancer. BE is a common condition in which normal stratified squamous epithelium of the esophagus is replaced with an intestine-like columnar epithelium, and it is the most prominent risk factor for EAC. This review aims to impartially systemize the knowledge from a large number of publications that describe the molecular and biochemical alterations occurring over this progression sequence. In order to provide an unbiased extraction of the knowledge from the literature, a text-mining methodology was used to select genes that are involved in the BE progression, with the top candidate genes found to be TP53, CDKN2A, CTNNB1, CDH1, GPX3, and NOX5. In addition, sample frequencies across analyzed patient cohorts at each stage of disease progression are summarized. All six genes are altered in the majority of EAC patients, and accumulation of alterations correlates well with the sequential progression of BE to cancer, indicating that the textmining method is a valid approach for gene prioritization. This review discusses how, besides being cancer drivers, these genes are functionally interconnected and might collectively be considered a central hub of BE progression.

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A study to determine plasma antioxidant concentrations in patients with Barrett’s oesophagus

Cited by 11 publications

References 24 publications

Dietary intake of vegetables, folate, and antioxidants and the risk of Barrett’s esophagus

Dietary intake of vegetables, folate, and antioxidants and the risk of Barrett’s esophagus

Dietary Antioxidants, Fruits, and Vegetables and the Risk of Barrett's Esophagus

Overview of major molecular alterations during progression from Barrett's esophagus to esophageal adenocarcinoma

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