Duodenal diazepam-binding protein expression and plasma cholecystokinin after alcoholic pancreatitis.

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.