COMPARISSON OF PREVALENCE OF ESOPHAGEAL MOTILITY DISORDERS IN PATIENTS WITH AND WITHOUT GASTROESOPHAGEAL REFLUX DISEASE

The pathogenic basis of gastroesophageal reflex (GERD) is multifactorial. The role of lower esophageal sphincter has been studied extensively. Since peristalsis governs esophageal acid clearance, recently researchers paid attention to the role of esophageal peristalsis in GERD. This study evaluates the relationship between esophagitis, esophageal acid exposure and manometric indicators of esophageal motility. A total of 55 patients were divided in three groups according to endoscopic, manometric and on a 24 hr pH values: group 1- patient with esophagitis (n = 18), group 2- patients with GERD without esophagitis (Non-erosive reflex disease, NERD, n = 17) and group 3- patients without GERD (control, n = 20).. Manometric data collected included measurement of the lower esophageal sphincter (LES) pressure, amplitude and duration of esophageal contractions and ineffective esophageal motility (defined as amplitude of contraction less than 30 mmHg at distal esophagus or non-transmitting contractions after >30 % of wet swallowing) were compared in all these groups.The results showed that mean resting LES pressures were 24.49, 33.47 and 32.91 mmHg in groups 1, 2 and 3 respectively, showing no significant differences between the three groups (p>0.05). Furthermore, there were no significance differences in mean duration of contractions between the groups (p>0.05). However, the amplitude of contractions was lower in esophagitis group and NERD group relative to control group (p<0.001). In addition, non-peristaltic contractions were more frequent in esophagitis and NERD groups than in the control group. Ineffective esophageal motility was seen in 72.2 % of patients in esophagitis group, 23 % of NERD group and 5 % of controls (P < 0.001). These results show that the resting LES pressure has no significant role in GERD. Furthermore, esophageal hypomotility was more prevalent in GERD and may have an important role in pathogenesis and severity determinant of GERD.