Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The level and functional activity of the major protease inhibitors in plasma and faecal extracts were analysed in 26 consecutive patients admitted during their first attack of acute severe colitis. The patients were retrospectively divided into two groups: one with total colitis and another with distal colitis. The patients with total colitis had a significantly lower alpha 2-macroglobulin level in plasma than normal individuals and patients with distal disease, whereas no difference in the levels of alpha 1-protease inhibitor, antichymotrypsin, antithrombin III, and alpha 2-antiplasmin was noted between the two groups. The protease-inhibiting capacity was saturated, and free proteolytic activity was present in the faecal extracts. In the extracts complex formation was demonstrated between leukocyte proteases and the antiproteases alpha 1-protease inhibitor and alpha 2-macroglobulin. It is concluded that the low plasma level of alpha 2-macroglobulin in patients with severe total colitis is mainly due to a consumption caused by complex formation with proteases, as earlier demonstrated in patients with acute pancreatitis and sepsis.
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PMID:Protease inhibitors in plasma and faecal extracts from patients with active inflammatory bowel disease. 242 96

The concentration of the pancreatic secretory trypsin inhibitor (PSTI) was measured in serum from 360 patients with acute abdominal diseases. Elevated levels were found in acute pancreatitis, cholangitis, choledocholithiasis, acute cholecystitis, pancreatic pseudocyst, malignancy, renal failure and in several different inflammatory conditions not connected with the pancreas. The results suggest the possibility of an extra-pancreatic production of PSTI, especially since the changes seen over time do not favour leakage or reabsorption as the cause of the high PSTI levels seen in acute pancreatitis. PSTI rather behaves as an acute phase reactant, as judged from the parallelism in the reaction pattern with antichymotrypsin.
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PMID:Serum levels of immunoreactive PSTI in acute abdominal disorders, with special reference to a possible extrapancreatic PSTI production. 243 67

The interaction of human pancreatic chymotrypsin A with serum inhibitors was assessed by enzyme immunoassay, enzymatic activity and inhibitory capacity measurements and electrophoretic analyses. In normal serum, chymotrypsin A was detected in four forms: one form (Mr approximately equal to 25,000) which might be chymotrypsinogen A and three forms complexed to the main inhibitors present in serum, alpha 2-macroglobulin (alpha 2-M), alpha 1-proteinase inhibitor (alpha 1-PI) and alpha 1-antichymotrypsin (alpha 1-Achy). As chymotrypsin A remains to 90% active when bound to alpha 2-M, the chymotrypsin A/alpha 2-M complex was quantified by an enzymatic assay. The kinetic parameters of the interaction of chymotrypsin A with alpha 1-PI and alpha 1-Achy were determined. Using these data the partition of chymotrypsin A between the different inhibitors in serum was calculated. In acute pancreatitis, the chymotrypsin A plasma level follows the progression of the disease and in this case as well as in normal serum alpha 1-PI is the major antagonist of chymotrypsin A.
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PMID:"In vivo" and "in vitro" inhibition of human pancreatic chymotrypsin A by serum inhibitors. 243 3

Extrapancreatic findings at computed tomography (CT), performed within 24 h in 42 consecutive episodes of acute pancreatitis, were classified according to a scoring system (EP score) and were correlated to Ranson's prognostic signs, to duration of hospital stay, biochemical changes in plasma and pancreatic ischaemia found at CT with contrast enhancement. Increasing EP score was found to be related to increasing number of positive Ranson's signs, longer hospital stay and pancreatic ischaemia. Plasma levels of immunoreactive cationic trypsin and amylase were not proportional to EP score. alpha 1-protease inhibitor, antichymotrypsin but not immunoreactive pancreatic secretory trypsin inhibitor increased proportionally to EP score. No changes related to EP score were seen in alpha 2-macroglobulin levels. Serum levels of trypsin-alpha 1-protease inhibitor complex were maximal after 3 days and most pronounced in cases with high EP scores. Plasma levels of factor X, alpha 2-antiplasmin and C1-esterase inhibitor were found to be inversely proportional to EP score.
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PMID:Pathobiochemistry and early CT findings in acute pancreatitis. 248 91

Serial measurements of circulating antiproteases were carried out on 42 consecutive patients admitted with acute pancreatitis. In the 7 days following admission the serum levels of alpha 1 antitrypsin (alpha 1 AT), alpha 1 antichymotrypsin (alpha 1 ACT) and the trypsin inhibitory capacity (TIC) increased by more than 300 per cent. The serum concentration of alpha 2 macroglobulin (alpha 2 M) alone showed a decline which was most profound in those patients with severe acute pancreatitis. Initial experience of fresh frozen plasma as a source of extrinsic antiproteases in severe acute pancreatitis is that it fails to prevent the decline in alpha 2 M or increase the already elevated TIC of the patients' serum.
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PMID:Antiprotease capacity in acute pancreatitis. 376 47

A clinical and biochemical analysis of 27 attacks of acute pancreatitis was made throughout the course of the disease. In severe attacks alpha 2-macroglobulin (alpha 2-M) decreased during the first days, reaching values in blood below 40% of the normal value. In addition, this remaining alpha 2-M had a decreased trypsin-binding capacity, indicating circulating alpha 2-M protease complexes. The inter-alpha-trypsin inhibitor concentration was also decreased, whereas alpha 1-proteinase inhibitor, antichymotrypsin, and pancreatic secretory trypsin inhibitor increased. All changes were most pronounced in the peritoneal fluid and were also closely correlated to the severity of the disease, assessed by both Ranson's and McMahon's classification systems. All patients with clinical complications had profound biochemical changes. In accordance with earlier findings, activation of both the complement and kinin systems seems possible in both blood and peritoneal fluid at the low alpha 2-M concentrations found in severe attacks.
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PMID:Protease inhibitors in acute human pancreatitis. Correlation between biochemical changes and clinical course. 608 96

alpha 2-macroglobulin is probably the most important of the antiproteases in plasma. In this study, the relationships of plasma alpha 2-macroglobulin to the clinical features of acute pancreatitis as well as to plasma levels of other antiproteases, immunoglobulins, and immunoreactive trypsin, were investigated in 55 patients with acute pancreatitis. The mean level of alpha 2-macroglobulin in 395 plasma samples from the patients was 2.12 g/liter compared with 2.41 g/liter in 29 healthy subjects and 2.93 g/liter in 17 patients with septicemia. Plasma levels were lower in 12 patients with severe pancreatitis than in 43 with mild attacks, and the lowest levels in three fatal attacks were less than half the mean of the normal range. Lowest levels were recorded at a mean time of 3 days after admission in the patients with mild attacks, at 5 days after admission in the patients with severe attacks, and 9 days after admission in those with fatal attacks. In contrast, plasma levels of the alpha 1-proteinase inhibitor antichymotrypsin and C-reactive protein increased to above normal levels during the attack, significantly more so in severe compared with mild attacks. Plasma levels of IgA, IgG, and IgM remained within the normal range or were increased. In patients with severe pancreatitis, plasma levels of immunoreactive trypsin remained elevated for longer than in those with mild attacks although there was little initial difference in the levels. These data suggest that decreasing levels of alpha 2-macroglobulin during the course of acute pancreatitis are due to a specific mechanism and unrelated, for the most part, to any generalized effect of pancreatitis on protein synthesis. The formation of rapidly cleared complexes between alpha 2-macroglobulin and active proteases is the most tenable explanation for the depletion of plasma levels, but the clinical significance of the changes remains unclear.
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PMID:Relation of alpha 2-macroglobulin and other antiproteases to the clinical features of acute pancreatitis. 619 93

An evaluation of C reactive protein as an indicator of the progress of acute pancreatitis has been made, and the data have been compared with the information given by the white cell count, erythrocyte sedimentation rate, and temperature and by two antiproteases--alpha 1 protease inhibitor and alpha 1 antichymotrypsin. The main value of C reactive protein is to provide a guide to the severity of the inflammation and to increase clinicians' awareness of the patient's enhanced risk of developing pancreatic collections when the C reactive protein concentration remains high (greater than 100 mg/l) at the end of the first week of the illness. In this respect C reactive protein concentrations are superior to white cell count, erythrocyte sedimentation rate, and temperature and the concentrations of antiproteases.
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PMID:C reactive protein: an aid to assessment and monitoring of acute pancreatitis. 654 92