Lori A Fischbach1, David Y Graham2, Jennifer R Kramer3, Massimo Rugge4, Gordana Verstovsek5, Paola Parente4, Abeer Alsarraj6, Stephanie Fitzgerald6, Yasser Shaib2, Neena S Abraham7, Anna Kolpachi8, Swapna Gupta8, Marcelo F Vela2, Maria Velez2, Rhonda Cole2, Bhupinderjit Anand2, Hashem B El Serag9. 1. 1] Department of Epidemiology, University of North Texas Health Science Center, Fort Worth, Texas, USA [2] Department of Epidemiology, University of Arkansas for Medical Sciences, College of Public Health, Little Rock, Arkansas, USA. 2. Michael E. DeBakey VA Medical Center, Department of Medicine, Section of Gastroenterology and Hepatology, Houston, Texas, USA. 3. 1] Michael E. DeBakey VA Medical Center, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA [2] VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey VA Medical Center, Baylor College of Medicine Section of Health Services Research, Houston, Texas, USA. 4. Surgical Pathology & Cytopathology Unit, Department of Diagnostic Medical Sciences & Special Therapies, University of Padova, Padova, Italy. 5. Department of Pathology, Michael E. DeBakey VA Medical Center, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA. 6. 1] Michael E. DeBakey VA Medical Center, Department of Medicine, Section of Gastroenterology and Hepatology, Houston, Texas, USA [2] Michael E. DeBakey VA Medical Center, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA [3] VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey VA Medical Center, Baylor College of Medicine Section of Health Services Research, Houston, Texas, USA. 7. 1] Michael E. DeBakey VA Medical Center, Department of Medicine, Section of Gastroenterology and Hepatology, Houston, Texas, USA [2] VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey VA Medical Center, Baylor College of Medicine Section of Health Services Research, Houston, Texas, USA. 8. Primary Care, Michael E. DeBakey VA Medical Center, Department of Medicine, Houston, Texas, USA. 9. 1] Michael E. DeBakey VA Medical Center, Department of Medicine, Section of Gastroenterology and Hepatology, Houston, Texas, USA [2] VA HSR&D Center for Innovations in Quality, Effectiveness and Safety, Michael E. DeBakey VA Medical Center, Baylor College of Medicine Section of Gastroenterology and Hepatology, Houston, Texas, USA.
Abstract
OBJECTIVES: The estimated association between Helicobacter pylori and Barrett's esophagus (BE) has been heterogenous across previous studies. In this study, we aimed to examine the association between H. pylori and BE and to identify factors that may explain or modify this association. METHODS: We conducted a case-control study in which we used screening colonoscopy controls recruited from primary care clinics as our primary control group in order to minimize selection bias. All participants underwent an esophagogastroduodenoscopy with gastric mapping biopsies. We used logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs) to estimate the association between H. pylori and BE while controlling for confounders. RESULTS: We identified 218 cases and 439 controls. The overall OR for the association between H. pylori and BE after controlling for age and white race was 0.55 (95% CI: 0.35-0.84). We observed an even stronger inverse association (OR: 0.28; 95% CI: 0.15, 0.50) among participants with corpus atrophy or antisecretory drug use ≥ 1 time per week (factors thought to lower gastric acidity), and no inverse association in patients without these factors (OR: 1.32; 95% CI: 0.66, 2.63). CONCLUSIONS: The association between H. pylori and a decreased risk for BE appears to occur in patients with factors that would likely lower gastric acidity (corpus atrophy or taking antisecretory drugs at least once a week).
OBJECTIVES: The estimated association between Helicobacter pylori and Barrett's esophagus (BE) has been heterogenous across previous studies. In this study, we aimed to examine the association between H. pylori and BE and to identify factors that may explain or modify this association. METHODS: We conducted a case-control study in which we used screening colonoscopy controls recruited from primary care clinics as our primary control group in order to minimize selection bias. All participants underwent an esophagogastroduodenoscopy with gastric mapping biopsies. We used logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs) to estimate the association between H. pylori and BE while controlling for confounders. RESULTS: We identified 218 cases and 439 controls. The overall OR for the association between H. pylori and BE after controlling for age and white race was 0.55 (95% CI: 0.35-0.84). We observed an even stronger inverse association (OR: 0.28; 95% CI: 0.15, 0.50) among participants with corpus atrophy or antisecretory drug use ≥ 1 time per week (factors thought to lower gastric acidity), and no inverse association in patients without these factors (OR: 1.32; 95% CI: 0.66, 2.63). CONCLUSIONS: The association between H. pylori and a decreased risk for BE appears to occur in patients with factors that would likely lower gastric acidity (corpus atrophy or taking antisecretory drugs at least once a week).
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