TY - JOUR
T1 - Infusion of C1-inhibitor plasma concentrate prevents hyperamylasemia induced by endoscopic sphincterotomy
AU - Testoni, Pier Alberto
AU - Cicardi, Marco
AU - Bergamaschini, Luigi
AU - Guzzoni, Simona
AU - Cugno, Massimo
AU - Buizza, Mario
AU - Bagnolo, Francesco
AU - Agostoni, Angelo
PY - 1995
Y1 - 1995
N2 - 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. (Gastrointest Endosc 1995;42:301-5.).
AB - 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. (Gastrointest Endosc 1995;42:301-5.).
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U2 - 10.1016/S0016-5107(95)70126-5
DO - 10.1016/S0016-5107(95)70126-5
M3 - Article
C2 - 8536896
AN - SCOPUS:0028809802
VL - 42
SP - 301
EP - 305
JO - Gastrointestinal Endoscopy
JF - Gastrointestinal Endoscopy
SN - 0016-5107
IS - 4
ER -