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. 2001 Apr;32(4):471-4.
doi: 10.1097/00005176-200104000-00015.

Delayed gastric emptying and gastroesophageal reflux: a pathophysiologic relationship

Affiliations

Delayed gastric emptying and gastroesophageal reflux: a pathophysiologic relationship

J Estevão-Costa et al. J Pediatr Gastroenterol Nutr. 2001 Apr.

Abstract

Background: Delayed gastric emptying (DGE) is frequent in patients with gastroesophageal reflux (GER), but its pathophysiologic role has not yet been established. To identify a relationship between DGE and GER, we assessed whether DGE increases esophageal acid exposure and the related importance of possible mechanisms.

Methods: Thirty pediatric patients with pathological GER were divided according to gastric emptying scintigraphy into a DGE group (n = 14) and normal-emptying group (n = 16). The esophageal pH-monitoring parameters of the two groups were compared with respect to the individual variation between postprandial and fasting periods.

Results: Patients with DGE had less total acid exposure than did those with normal emptying, but patients in both groups had a pathological fraction of time when pH was below 4 in both the postprandial (median: 18 vs. 27.6; P = 0.49) and fasting (8.5 vs. 23.9; P = 0.01) periods. Patients in the normal-emptying group had similar fraction of time when pH was below 4 in the postprandial and fasting periods. However, patients in the group with DGE had a fraction of time when pH was below 4 in the postprandial period that was almost double that presented in fasting period (postprandial to fasting ratio: 2.11:0.90; P = 0.002). The postprandial to fasting ratio for episodes per hour was similar in the two groups (1.81 vs. 1.79; P = 0.62). Patients with DGE had a significantly higher frequency of long episodes in the postprandial period than did those with normal emptying (62.5% vs. 38.2%; P = 0.04). The occurrence of the longest episode in the postprandial period was also significantly higher for patients with DGE (57.1% vs. 6.2%; P = 0.003).

Conclusions: DGE seems to accentuate postprandial reflux by increasing the volume of refluxate per episode of reflux through an underlying incompetent lower esophageal sphincter.

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