AIM: Chronic nonpathological pancreatic hyperenzymemia (CNPH) is a new syndrome characterized by an increase in serum pancreatic enzymes in the absence of pancreatic disease. The aim of this study was to increase our understanding of this condition by determining the serum pancreatic enzyme response as well as changes in the caliber of the Wirsung duct after secretin stimulation. METHODS: Twenty subjects with CNPH and 9 healthy subjects without CNPH were studied. Blood samples were drawn 5 and 0 min before and 5, 10, 15, 30, 45, and 60 min after intravenous injection of secretin (1 U/kg). Amylase, pancreatic isoamylase, and lipase concentrations were determined. The caliber of the Wirsung duct was measured by ultrasonography. RESULTS: The injection of secretin caused a marked and statistically significant (p < 0.05) increase in serum pancreatic enzymes in the subjects with CNPH that persisted for the duration of the study. The increase over the basal value was in the range of 1.2- to 1.6-fold for amylase, 1.4- to 2.1-fold for pancreatic isoamylase, and 2.6- to 4.2-fold for lipase. In the control subjects the increase was mild, but statistically significant (p < 0.05), ranging from 1.1- to 1.2-fold for amylase, 1.2- to 1.4-fold for pancreatic isoamylase, and 1.5- to 2.2-fold for lipase. The injection of secretin caused a slight increase in the diameter of the Wirsung duct in both groups of subjects, but this was statistically significant only during the first 30 min of the study. CONCLUSIONS: The serum pancreatic enzyme response to secretin was more marked in CNPH than in controls. The Wirsung duct showed no alterations after secretin injection that would help to explain the hyperenzymemia. Copyright 2003 S. Karger AG, Basel and IAP
AIM: Chronic nonpathological pancreatic hyperenzymemia (CNPH) is a new syndrome characterized by an increase in serum pancreatic enzymes in the absence of pancreatic disease. The aim of this study was to increase our understanding of this condition by determining the serum pancreatic enzyme response as well as changes in the caliber of the Wirsung duct after secretin stimulation. METHODS: Twenty subjects with CNPH and 9 healthy subjects without CNPH were studied. Blood samples were drawn 5 and 0 min before and 5, 10, 15, 30, 45, and 60 min after intravenous injection of secretin (1 U/kg). Amylase, pancreatic isoamylase, and lipase concentrations were determined. The caliber of the Wirsung duct was measured by ultrasonography. RESULTS: The injection of secretin caused a marked and statistically significant (p < 0.05) increase in serum pancreatic enzymes in the subjects with CNPH that persisted for the duration of the study. The increase over the basal value was in the range of 1.2- to 1.6-fold for amylase, 1.4- to 2.1-fold for pancreatic isoamylase, and 2.6- to 4.2-fold for lipase. In the control subjects the increase was mild, but statistically significant (p < 0.05), ranging from 1.1- to 1.2-fold for amylase, 1.2- to 1.4-fold for pancreatic isoamylase, and 1.5- to 2.2-fold for lipase. The injection of secretin caused a slight increase in the diameter of the Wirsung duct in both groups of subjects, but this was statistically significant only during the first 30 min of the study. CONCLUSIONS: The serum pancreatic enzyme response to secretin was more marked in CNPH than in controls. The Wirsung duct showed no alterations after secretin injection that would help to explain the hyperenzymemia. Copyright 2003 S. Karger AG, Basel and IAP