Background: A high dose of cholecystokinin (CCK) agonist cerulein can induc
e acute pancreatitis in animals. The role of CCK in the induction of acute
pancreatitis in humans is unclear. We investigated basal plasma CCK levels
before and after induction of post-ERCP pancreatitis to determine CCK level
s in the early course of the disease.
Study Design: We determined plasma CCK concentrations in four groups of pat
ients who underwent ERCP: (1) post-ERCP pancreatitis patients (n = 23); (2)
patients with post-ERCP hyperamylasemia without pancreatitis (n = 5); (3)
patients with post-ERCP abdominal pain without hyperamylasemia (n = 18); an
d (4) patients with an uneventful post-ERCP period (n = 43). Plasma samples
were taken before ERCP, 4 to 8 hours, 10 to 16 hours, and 24 hours after E
RCP. Plasma CCK concentrations were determined by a specific and sensitive
radioimmunoassay using CCK antiserum (Euro-Diagnostica, Malmo, Sweden).
Results: Plasma CCK levels increased five-fold early in the course in post-
ERCP pancreatitis patients, but not in post-ERCP hyperamylasemia patients o
r in uncomplicated ERCP patients, where CCK levels temporarily decreased af
ter ERCP. In patients with abdominal pain, CCK levels did not change. After
the early increase, plasma CCK levels declined to almost unmeasurable leve
ls one day after the onset of symptoms in post-ERCP pancreatitis. In other
groups CCK levels were close to the pre-ERCP level.
Conclusions: It remains to be shown whether CCK is important in the pathoge
nesis of post-ERCP pancreatitis or merely a secondary phenomenon. There is
a rationale to test CCK antagonists in preventing post-ERCP pancreatitis. (
J Am Coll Surg 1999;189:560-565. (C) 1999 by the American College of Surgeo
ns).