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Medline ® Abstract for Reference 141

of 'Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis'

141
TI
Infusion of C1-inhibitor plasma concentrate prevents hyperamylasemia induced by endoscopic sphincterotomy.
AU
Testoni PA, Cicardi M, Bergamaschini L, Guzzoni S, Cugno M, Buizza M, Bagnolo F, Agostoni A
SO
Gastrointest Endosc. 1995;42(4):301.
 
Hyperamylasemia after endoscopic sphincterotomy is a common event, occurring in about 70% of cases. Clinical acute pancreatitis may also develop in 1% to 6% of cases. Previous attempts to prevent this reaction with inhibitors of exocrine pancreatic secretion (somatostatin and octreotide) provided conflicting and often disappointing results. Kallikrein is one of the proteases that sustain the inflammatory process in acute pancreatitis; the C1 inhibitor is the only physiologic inhibitor of the first component of the human complement cascade and is a major inactivator of kallikrein and Factor XII. Therefore, we tested the C1 inhibitor in the prevention of hyperamylasemia in 40 consecutive patients undergoing endoscopic sphincterotomy for common bile duct stones or benign papillary stenosis. They were given either C1 inhibitor (20 cases) or placebo (20 cases) before the procedure. Serum amylase levels were determined at baseline and 2, 4, 8, and 24 hours thereafter. Significant differences in serum amylase levels between groups were observed at 2 hours (p<.01), 4 hours (p<.0005), and 8 hours (p<.005) after sphincterotomy. The differences in amylase levels were also significant among the 24 subjects with pancreatic ductal filling (2 hours, p<.05; 4 hours, p<.005; 8 hours, p<.01) and the 9 patients with previous episodes of acute pancreatitis (4 hours,p<.05; 8 hours, p<.05; 24 hours, p<.05). The infusion of C1-inhibitor plasma concentrate resulted in a 50% increase in functional levels of C1 inhibitor (in the 8 cases for whom they were assayed), which persisted throughout the observation period.
AD
Institute of Internal Medicine, University of Milan, Italy.
PMID