J. U. Nguyen1, K. Feng1, J. P. Callaway2, B. L. Corey1, J. M. Grams1 1University Of Alabama at Birmingham,Division Of Gastrointestinal Surgery/Department Of Surgery,Birmingham, Alabama, USA 2University Of Alabama at Birmingham,Department Of Medicine,Birmingham, Alabama, USA
Introduction: Patients with obesity have been shown to have an increased intra-abdominal pressure and dysfunction of the gastroesophageal junction. We hypothesized that obesity would be associated with increased mean basal and residual lower esophageal sphincter (LES) pressures but also increased GERD.
Methods: Retrospective review was performed on all adult patients undergoing high resolution manometry (HRM) and 24-hour pH monitoring at a single academic institution from 2014 to 2016. Exclusion criteria included a diagnosis of achalasia or hiatal hernia, and active acid suppression medications during testing. Patients were stratified by BMI (kg/m2): normal weight <25; overweight 25 to 29.9; class I, II, class III obesity at 30 to 34.9, 35-39.9, and ≥ 40, respectively. Statistical analyses were performed using Chi-square test, Kruskal-Wallis one-way analysis of variance, linear regression, or multiple regression as appropriate. Statistical significance was determined as p-value <0.05.
Results: A total of 507 patients were included in the study. After stratification, there were 149 (29.4%) patients who had normal weight, 159 (31.4%) overweight, 121 (23.9%) with class I obesity, 46 (9.1%) with class II obesity, and 32 (6.3%) with class III obesity. Mean basal LES pressure was significantly increased in patients with class III obesity (p=0.004), while mean residual LES pressure only trended toward being increased (p=0.060). There was no statistical difference in esophageal contraction vigor (Distal Contractile Integral, DCI) (p=0.43). In unadjusted linear regression models, there was a positive linear correlation between mean basal LES pressure and BMI (p<0.001) as well as between mean residual LES pressure and BMI (p<0.001). There was no association between DCI and BMI (p=0.425). These results persisted after adjustment for age. In subset analyses, 24-h pH monitoring was performed in 201 of these patients: normal weight 54 (26.9%), overweight 67 (33.3%), obesity 80 (39.8%). There were no significant differences among the groups in any esophageal acid exposure parameters or between any of the parameters of esophageal acid exposure and BMI when examined as a continuous variable.
Conclusion: In conclusion, these data suggest that obesity augments the basal resting and relaxation pressures of the LES but is not associated with changes in esophageal contractility. However, mean DCI values in obesity still remained within normal limits and standard criteria should be adequate to determine disease states. Obesity did not result in increased esophageal acid exposure.
