Duodenal diazepam‐binding protein expression and plasma cholecystokinin after alcoholic pancreatitis

Abstract

Objective. After the first acute alcohol‐induced pancreatitis (AAIP) episode 46 % of patients will have a recurrent attack, but the pathophysiology is unclear. The hyperstimulation of the pancreas with cholecystokinin (CCK) induces acute pancreatitis. Alcohol induces temporary stimulation of the pancreas and CCK could be a mediator. CCK is regulated by releasing peptides – diazepam‐binding protein (DBI) being a possible candidate. The aim of this study was to investigate the possible association between CCK plasma levels and DBI expression in patients with AAIP or its recurrence. Material and methods. The study comprised 44 subjects (mean age 42 years): A) Patients with a first episode of AAIP (n = 9); B) patients with three or more episodes of AAIP (n = 11); C) patients with a heavy alcohol consumption, with no detected AAIP (n = 11) and D) healthy controls (n = 13). CCK levels were measured by radioimmunoassay (RIA). Duodenal biopsies were analyzed for DBI mRNA and histology. Results. There was no significant difference in CCK plasma levels, DBI expression or CCK/DBI ratio between the groups. Conclusions. There were no changes in fasting CCK plasma levels or DBI expression. This may suggest that they do not play a major role as risk factors for alcohol‐induced pancreatitis.

• Acute and recurrent pancreatitis
• alcohol‐induced pancreatitis
• cholecystokinin‐releasing peptide

Acknowledgements

This work was supported in part by grants from the Mary and Georg C Ehrnrooth Foundation, the AstraZeneca Corporation Research Foundation, the Orion Corporation Research Foundation, the Yrjö Jahnsson Foundation and the Medical Research Fund of Tampere University Hospital.