Quantcast

Obesity increases the risk of erosive esophagitis but metabolic unhealthiness alone does not: a large-scale cross-sectional study.

Research paper by Myong Ki MK Baeg, Sun-Hye SH Ko, Seung Yeon SY Ko, Hee Sun HS Jung, Myung-Gyu MG Choi

Indexed on: 10 Jun '18Published on: 10 Jun '18Published in: BMC gastroenterology



Abstract

Obesity is a known risk factor for erosive esophagitis (EE) and metabolic unhealthiness has been implicated in EE pathogenesis. However, obesity and metabolic unhealthiness are not synonymous and the associations between obesity, metabolic health, and EE are unclear. Therefore, our aim was to investigate the relationship between EE, obesity, and metabolic health. We performed a retrospective cross-sectional study of subjects undergoing health screening at a university hospital. Subjects were classified into 4 groups based on metabolic and obesity criteria: metabolically healthy nonobese (MHNO), metabolically healthy obese (MHO), metabolically unhealthy nonobese (MUNO), and metabolically unhealthy obese (MUO). Multivariable analysis was used to identify EE risk factors with MHNO subjects as reference. To determine if there were synergistic interactions between metabolic health and obesity status, the Rothman's synergy index and attributable proportion of risk were also calculated. We included 10,338 subjects (5448 MHNO, 1605 MHO, 1600 MUNO, 1685 MUO). The prevalence of EE was 6.5% in MHNO, 12.6% in MHO, 9.3% in MUNO, and 14.3% in MUO. EE risk was increased significantly by obesity (MHO: OR, 1.589, 95% CI, 1.314-1.921, P < 0.001; MUO: OR, 1.734, 95% CI, 1.441-2.085, P < 0.001), but not in MUNO subjects (OR, 1.224, 95% CI, 0.991-1.511, P = 0.060). Male sex, blood leukocyte count, alcohol, and smoking significantly increased EE risk, but H. pylori infection was protective. Replacement of obesity with abdominal obesity gave similar results. The Rothman's synergy index was 0.920 (95% CI, 0.143-5.899) and the attributable proportion of risk was - 0.051 (95% CI, - 1.206-1.105), indicating no interaction between metabolic and obesity status on EE risk. We demonstrated that obesity increased the risk of EE, regardless of metabolic health status. However, EE risk was not significantly increased in MUNO subjects, suggesting that metabolic unhealthiness may not be involved in EE pathogenesis. As observational cross-sectional studies cannot prove causality, prospective longitudinal studies involving obesity and metabolic treatment should be performed to further investigate the association between obesity, metabolic health, and EE risk.