Abstract

Background: Patients with alcohol-related chronic pancreatitis (ARCP) may have accelerated mouth-to-cecum transit, particularly in the presence of autonomic neuropathy. Nevertheless, the roles of gastric emptying (GE) and transit throughout proximal and distal small bowel in the origin of the abnormal gastrointestinal transit (GIT) in ARCP have not been much studied. Aim: To assess GIT and to determine the roles of GE and segmental transit throughout the proximal and the distal small bowel in ARCP patients. Method: Eighteen healthy controls and 40 male ARCP patients were studied, including 17 with diabetes mellitus and malabsorption, 10 with diabetes only, 3 with malabsorption only and 10 without diabetes or malabsorption. Autonomic neuropathy was detected in 20 patients by standardized cardiovascular tests. GIT was assessed by scintigraphy after ingestion of a liquid meal labeled with 99mTechnetium-phytate and defined as the time of meal arrival to the cecum. Abdominal scans were serially taken for 180 min with a gamma camera. Counts for regions of interest defined for the stomach, proximal and distal small bowel, and cecum yield data for calculation for GE half-time, and the times of meal arrival to the proximal and to the distal small bowel and the cecum. Accumulation of the meal in the distal small bowel was estimated as the proportion of ingested radioactivity found in this region by the time that cecum filling started. Results: GIT was significantly shorter (p 180min vs 102min; 50->180min) and 11 patients were considered as having definite abnormally accelerated GIT. There were no significant differences (p>0.20) between patients and controls concerning GE half-time (50min; 5-13min vs 55min; 16-83min). There were also no differences (p>0.50) between patients and controls regarding the times of meal arrival to the proximal (15min; 1-45min vs 13min; 3-70min) and distal small bowel (23min; 4-64min vs 30min; 12-83min). However, accumulation of the meal in the distal small bowel was lower (p 0.1). Univariate analysis showed that rapid GIT is associated with both impaired accumulation of the meal in the distal small bowel (7/11 vs 3/29; p=0.001) and autonomic neuropathy (10/11 vs 10/29; p= 0.003). Conclusion: Abnormally rapid GIT in ARCP patients does not seem to be due to accelerated GE but is related to impaired accumulation of the meal in the distal small bowel and to autonomic neuropathy.

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