pancreatic pseudocyst/protease

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Pancreatic pseudocysts: a biochemical evaluation of proteases and protease inhibitors in plasma.

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A biochemical evaluation was performed on plasma from eight patients developing a pancreatic pseudocyst during acute pancreatitis attacks and from six patients with a known pseudocyst. Patients developing an acute pancreatic pseudocyst had high levels of activated trypsin in complex with alpha

Proteolytic activity in pancreatic pseudocyst fluid.

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Pancreatic pseudocyst fluids from 15 patients were biochemically analyzed, especially concerning proteolytic activity and protease inhibitors, and correlated to the clinical course. The pseudocyst fluid was a mixture of pancreatic juice and plasma possessing a high proteolytic activity against high-

Pancreatic pseudocyst fluid--a mixture of plasma proteins and pancreatic juice possessing a high proteolytic activity.

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Pancreatic pseudocyst fluid from eight patients was examined biochemically. The fluid was found to be a mixture of plasma proteins and pancreatic juice, possessing a high proteolytic activity against high- as well as low-molecular-weight proteins. The proteolytic activity was found to be trypsin-,

Pancreatic pseudocyst after acute organophosphate poisoning.

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Acute organophosphate poisoning (OP) shows several severe clinical symptoms due to its strong blocking effect on cholinesterase. Acute pancreatitis is one of the complications associated with acute OP, but this association still may not be widely recognized. We report here the case of a 73-year-old

The proteolytic effect of pancreatic pseudocyst fluid on vessel walls.

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The possible in vivo consequences of proteolytic activity found in pancreatic pseudocyst fluid was investigated experimentally using fresh vessels from rabbit and humans. Proteolytic pseudocyst fluid caused a pronounced and time-dependent decrease in breaking strength of fresh vessels. A destruction

Digestive enzymes and protease inhibitors in plasma from patients with acute pancreatitis.

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The plasma levels of certain digestive enzymes and protease inhibitors were determined in 40 patients with severe acute pancreatitis diagnosed as gallstone-induced (GP), alcoholic (AP), or idiopathic (IP). On admission, plasma levels of amylase and immunoreactive cationic trypsin(ogen) (IRCT) and

Alpha 1-antitrypsin deficiency and chronic pancreatitis.

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Alpha 1-antitrypsin deficiency is a genetic disorder commonly associated with pulmonary and hepatic injury. Low serum levels of this glycoprotein result in an imbalance between circulating protease and protease inhibitors, which is thought to play a role in the development of emphysema. In recent

The treatment of chronic recurrent pancreatitis with depot secretin--a preliminary report.

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Increased viscosity and raised lactoferrin, trypsin and protein concentrations in selectively aspirated pancreatic secretion, prompted us to try depot secretin therapy in patients with advanced chronic recurrent pancreatitis without pancreatic duct obstruction or pancreatic pseudocysts. The idea

Impaired mononuclear phagocyte function in patients with severe acute pancreatitis: evidence from studies of plasma clearance of trypsin and monocyte phagocytosis.

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Activated proteases in plasma are complexed by alpha 2-macroglobulin. Although the complexes retain peptidase activity, they are usually eliminated promptly by mononuclear phagocytes. In severe acute pancreatitis, almost 30% of plasma alpha 2-macroglobulin becomes complexed, suggesting impaired

Hereditary pancreatitis for the endoscopist.

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Hereditary pancreatitis shares a majority of clinical and morphologic features with chronic alcoholic pancreatitis, but may present at an earlier age. The term hereditary pancreatitis has primarily been associated with mutations in the serine protease 1 gene (PRSS1) which encodes for cationic

Comprehensive screening for PRSS1, SPINK1, CFTR, CTRC and CLDN2 gene mutations in Chinese paediatric patients with idiopathic chronic pancreatitis: a cohort study.

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OBJECTIVE Genetic alterations may contribute to chronic pancreatitis (CP) in Chinese young patients. This study was designed to investigate mutations of cationic trypsinogen (PRSS1), pancreatic secretory trypsin inhibitor or serine protease inhibitor Kazal type 1 (SPINK1), cystic fibrosis

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