Abstract
Background: Obesity is a known independent risk factor for both Barrett esophagus and esophageal adenocarcinoma. However, data about the effect of obesity on the risk of progression from nondysplastic Barrett esophagus to dysplasia or esophageal adenocarcinoma are lacking. The aim of this study was to evaluate whether obese patients with nondysplastic Barrett esophagus had a higher incidence of dysplasia development during routine surveillance than nonobese patients.Methods: In a retrospective review, 1,999 patients who had a first diagnosis of nondysplastic Barrett esophagus made by esophagogastroduodenoscopy (EGD) at a single community hospital were tracked to their surveillance EGD 3 to 5 years later to evaluate for dysplasia (low grade, high grade, or adenocarcinoma). We compared the incidence of dysplasia development in obese patients (body mass index [BMI] ≥30 kg/m2) with nonobese patients (BMI <30 kg/m2).Results: The sample population included 1,019 obese patients (51.0%) and 980 nonobese patients (49.0%) with nondysplastic Barrett esophagus. Their mean age was 56.5 ± 11.6 years, 1,228 (61.4%) were male, and 1,853 (92.7%) were Caucasian. At surveillance endoscopy performed at a mean follow-up of 3.7 years after their first EGD, 51 obese patients (incidence of 15.3 cases per 1,000 person-years, 95% confidence interval [CI], 11.5-19.9) and 15 nonobese patients (incidence of 4.6 cases per 1,000 person-years, 95% CI, 2.7-7.4) had developed dysplasia (P=0.0001).Conclusion: We found a significant increase in the incidence of dysplasia development in obese patients with nondysplastic Barrett esophagus at 3- to 5-year follow-up compared to nonobese patients. This finding suggests that more frequent surveillance in obese patients with nondysplastic Barrett esophagus may be warranted for early detection of dysplasia.
Highlights
Barrett esophagus is a known complication of chronic gastroesophageal reflux disorder (GERD); approximately 10% to 15% of patients with chronic GERD are diagnosed with Barrett esophagus.[1]
The carcinogenic mechanism by which obesity contributes to development of esophageal adenocarcinoma is not fully understood, but one proposal is that adipokines may alter esophageal mucosal injury healing in Barrett esophagus, leading to progression of the disease.[2]
At surveillance endoscopy 3 to 5 years after their first EGD demonstrating nondysplastic Barrett esophagus, 51 obese (5.0%) vs 15 nonobese (1.5%) patients had developed dysplasia, translating to a calculated incidence rate of dysplasia of 15.3 cases per 1,000 person-years in the obese population vs 4.6 cases per 1,000 person-years in the nonobese population
Summary
Barrett esophagus is a known complication of chronic gastroesophageal reflux disorder (GERD); approximately 10% to 15% of patients with chronic GERD are diagnosed with Barrett esophagus.[1]. The aim of this study was to evaluate whether obese patients with nondysplastic Barrett esophagus had a higher incidence of dysplasia development during routine surveillance than nonobese patients. Results: The sample population included 1,019 obese patients (51.0%) and 980 nonobese patients (49.0%) with nondysplastic Barrett esophagus Their mean age was 56.5 ± 11.6 years, 1,228 (61.4%) were male, and 1,853 (92.7%) were Caucasian. Conclusion: We found a significant increase in the incidence of dysplasia development in obese patients with nondysplastic Barrett esophagus at 3- to 5-year follow-up compared to nonobese patients. This finding suggests that more frequent surveillance in obese patients with nondysplastic Barrett esophagus may be warranted for early detection of dysplasia
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