FASTING AND POSTPRANDIAL MECHANISMS OF GASTROESOPHAGEAL REFLUX IN CHILDREN WITH GASTROESOPHAGEAL REFLUX DISEASE

In order to define the mechanisms of gastroesophageal reflux (GER) in children, we performed simultaneous intraluminal esophageal motility and pH studies in 24 children with symptomatic reflux and abnormal prolonged pH probe study, ten (group A) without endoscopic and histologic esophagitis, 14 (group B) with endoscopic and histologic esophagitis. Median (ranges) age (years) was 5.0 (6 months-10 years) and 3.0 (6 months-12 years), respectively. Recordings were done for 1 hr before and 1 hr after feeding apple juice (15 ml/kg; pH 4.0). All episodes of GER in group A patients and 77.1% in group B patients were accounted for by abrupt transient lower esophageal sphincter (LES) relaxation (TLESR); 22.9% of reflux events in group B patients occurred during gradual drifts of LES pressure (LESP) to undetectable levels. Esophageal refluxate exposure (mean percentage time with esophageal pH < 4.0), the rate of TLESR (number of episodes/hr), and the percentage of TLESRs associated with reflux significantly increased in the fed period both in group A (18.5 +/- 5.4%, 6.2 +/- 2.65, 87.1%) and in group B (29.7 +/- 6.5, 7.8 +/- 3.05, 84.9%) as compared to the fasting state (group A: 10.8 +/- 3.9, 3.9 +/- 3.17, 46.1%; group B: 16.1 +/- 2.6, 4.14 +/- 3.06, 55.17%) (p < 0.01). The rate of LESP drifts (number of episodes/hr) was also significantly higher postprandially (4.85 +/- 1.24 vs 1.8 +/- 0.9, p < 0.01); furthermore there was a postfeeding increase of the LESP drift percentage associated with reflux (79.41% vs 46.15%, p < 0.01). Residual pressure of TLESRs associated with reflux was significantly lower than that of TLESRs without GER in both groups of patients, during fasting (group A: p < 0.01; group B: p < 0.05) and fed state (p < 0.05), whereas duration of relaxation and LESP in the 1-min period before each TLESR did not discriminate TLESRs associated with reflux from those without reflux. In children with GER disease, TLESR is the most common mechanism of reflux, but gradual LESP drift is associated with more severe disease; the postprandial increase in the esophageal acid exposure is mainly due to increased rate of TLESRs and LESP drifts; degree of sphincter inhibition during TLESRs is a critical factor for the induction of reflux.