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

What Was Tested

Researchers studied Cholecystokinin (CCK) in the context of pancreatitis (after the acute phase) in this controlled clinical trial publication.

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.

Who Took Part

According to the abstract, 44 subjects were involved.

By PubMed's age tags, the people studied were adults, middle-aged adults and older adults, both men and women.

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).

How the Study Was Run

In design terms this was a pilot study.

It is described as a pilot, a small early test of whether a larger Cholecystokinin (CCK) study would be practical.

CCK levels were measured by radioimmunoassay (RIA).

Duodenal biopsies were analyzed for DBI mRNA and histology.

What Was Measured

Topics PubMed links to this paper include Alcoholism, Cholagogues and Choleretics, Cholecystokinin, Diazepam Binding Inhibitor, Duodenum, Pancreatitis, Alcoholic and Pilot Projects.

What This Means in Plain Language

The paper is a pilot study of Cholecystokinin (CCK) in 44 subjects in people with pancreatitis (after the acute phase).

Its findings take up roughly 3 sentences of the abstract and are left out here on purpose; the source paper is the place to read them.

The publication is from 2006 (Scandinavian journal of clinical and laboratory investigation), a journal based in England.

More context: the Cholecystokinin (CCK) compound page, Pancreatitis (after the acute phase) research.