%0 Journal Article
%T Manometric esophagogastric junction barrier metrics as predictors of gastroesophageal reflux.
%A Babbar S
%A Omara M
%A Khan A
%A Knotts R
%J Esophagus
%V 21
%N 3
%D 2024 Jul 1
%M 38691207
%F 3.671
%R 10.1007/s10388-024-01057-9
%X BACKGROUND: High-resolution manometry (HRM) tools, like esophagogastric junction contractile integral (EGJ-CI), assess EGJ barrier function.
OBJECTIVE: This study aimed to evaluate the relationships between manometric EGJ metrics with esophageal acid exposure.
METHODS: We conducted a retrospective review of 284 patients who underwent HRM and ambulatory reflux testing between 11/2017-1/2020. EGJ-CI and total-EGJ-CI were manually calculated. Pathologic acid exposure was defined as pH < 4 with esophageal acid exposure time (EAET) exceeding 6.0%. Pearson's correlation, univariable and multivariable regression models were utilized to assess the relationships between pathologic acid exposure and EGJ parameters. Sensitivity and specificity thresholds for EGJ-CI and total EGJ-CI were optimized with ROC analyses.
RESULTS: On univariable analysis, patients with pathologic acid exposure had increased odds of having lower mean basal LES pressures, EGJ-CI, and total EGJ-CI than patients without pathologic acid exposure. On multivariable analysis, age, EGJ-CI and mean DCI were significant predictors of pathologic acid exposure. There were significant, though weak, correlations between EAET and EGJ-CI and total EGJ-CI (r = - 0.18, - 0.19, p < 0.01, respectively). An EGJ-CI cutoff of 44.16 as a predictor for pathologic acid exposure had a sensitivity of 46% and specificity of 42% (AUC 0.60). Total EGJ-CI cutoff of 11,461.3 for pathologic acid exposure had a sensitivity of 44% and a specificity of 43% (AUC 0.62).
CONCLUSIONS: EGJ-CI can independently predict pathologic acid exposure. However, the poor correlation between EGJ-CI and acid exposure, as well as the low sensitivity and specificity of calculated thresholds, indicate that mechanisms other than EGJ barrier function may impact acid exposure.