Abstracts
Copyright ©The Author(s) 1996. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 1996; 2(Suppl1): 147-147
Published online Sep 15, 1996. doi: 10.3748/wjg.v2.iSuppl1.147
Esophageal motor pattern during fasting and postprandial states in non severe reflux esophagitis
Hui-Min Liu, Mei-Yun Ke, Zhi-Feng Wang, Cheng-Ming Gu, Yuan-Fang Chen
Hui-Min Liu, Mei-Yun Ke, Zhi-Feng Wang, Cheng-Ming Gu, Yuan-Fang Chen, Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China
Author contributions: All authors contributed equally to the work.
Received: December 11, 1995
Revised: February 21, 1996
Accepted: March 15, 1996
Published online: September 15, 1996
Abstract

AIM: It is well known that lower esophageal sphincter (LES) dysfunction is a key factor in development of gastroesophageal reflux disease (GERD), however, effective peristalsis is a critical determinant of esophageal acid clearance, The aims of our study were to investigate the LES pressure (LESP) and esophageal peristaltic function in patients with non severe reflux esophagitis (NSRE) during fasting and postprandial states.

METHODS: Ten patients with NSRE confirmed by endoscopy (grade I and II) and 10 age matched healthy subjects (HS) participated in this study. An upper gut manometry was performed with an 8 lumen Dent sleeve catheter through a capillary pneumohydraulic perfused system and polygraph. The catheter was positioned under fluoroscopy, 2 side holes at the antrum, 3 cm in interval, 3 side holes from the mid esophagus to distal esophagus, sleeve at LES area. Five hour recording was carried out, 3 h for fasting (migrating motor complex, MMC) and 2 h after meal. Swallows of water were used for evaluation of esophageal function.

RESULTS: (1) LESP during the phase I, II and of MMC were 23.3 ± 3.0, 29.2 ± 3.0, 53.4 ± 6.1 mmHg in HS and 16.1 ± 2.7, 30.5 ± 4.1, 43.4 ± 6.0 mmHg in NSRE. There were statistical significance among each phase in both group (P < 0.01). (2) LESP significantly decreased 1 h after meal in HS (11.75 ± 2.8 mmHg, vs phase I, P < 0.01), but not in NSRE (13.75 ± 3.37 mmHg, P = 0.59). (3) Primary peristaltic velocity (PV) in fasting significantly decreased in NSRE when compared with HS at the mid esophagus (2.48 ± 0.30 cm/s vs 4.10 ± 0.86 cm/s, P < 0.01) and the distal esophagus (3.16 ± 0.10 cm/s vs 1.78 ± 0.27 cm/s, P < 0.01). (4) Peristaltic wave duration (D) was prolonged in NSRE compared with HS at the middle (4.77 ± 0.26 s vs 3.36 ± 0.18 s, P < 0.01), the distal 1 (4.55 ± 0.24 s vs 3.59 ± 0.16 s, P < 0.01) and the distal 2 esophagus (3.95 ± 0.28 s vs 3.31 ± 0.23 s, P = 0.08). Wave amplitude (A) and PV decreased 1 h after meal when compared with HS at the mid esophagus (54.8 ± 7.4 mmHg vs 70.0 ± 6.0 mmHg, P = 0.12), the distal 1 (78.0 ± 9.2 mmHg vs 110.2 ± 7.7 mmHg, P < 0.01) and the distal 2 (62.35 ± 11.2 mmHg vs 94.55 ± 7.81 mmHg, P < 0.05), which remained similar at the 2nd hour in both groups. (5) Incidence of peristaltic contraction following water swallows were 88% at the mid esophagus and 47% at the diatal esophagus in NSRE, 88% (NS) and 70% (P < 0.05) in HS, respectively.

CONCLUSIONS: (1) Variations of LESP were similar in HS and NSRE groups, LESP could be normal, even increased, influenced by MMC activity and meal. (2) The abnormal changes predominantly appeared at the distal esophagus in NSRE. Our data suggested that dysfunction of esophageal primary peristalsis may result in acid clearance delay and play a more important role in the pathogenesis of NSRE.

Keywords: Reflux esophagitis; Esophageal manometry; Migrating motor complex