Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We propose a rapid enzymatic micromethod for the specific determination of lipase (EC 3.1.1.3) activity in serum and duodenal fluid. Free linoleic acid produced during 10-min incubation of 10 mul of sample with 1 ml of substrate (trillinolein emulsion) at 30 degrees C is converted by lipoxygenase (EC 1.99.2.1), in a coupled reaction, to its hydroperoxide, which is measured photometrically after solubilizing the reaction mixture in ethanol. Lipase activity is calculated from the rate of hydroperoxide formation, with linoleic acid as primary standard. The velocity of the reaction is greatest at pH 8.8, 35-37 degrees C, and a deoxycholate concentration of 3.6 mmol/liter. The energy of activation is 6.7 kcal/mol. The differing "apparent" Km values obtained for lipase in undiluted serum (4 X 10(-5) mol/liter) and in albumin-based diluents (1 X 10(-5) mol/liter) indicate the presence of a competitive inhibitor in the serum matrix. We detected no lipase activity in urine. Results by the proposed method correlate well with those by a copper soap extraction method (r = 0.95), but values are significantly higher for pancreatitis patients' sera (slope 1.6). The linear dynamic range extends to 1000 U/liter. Hemolysis, lipemia, and hyperbilirubinemia do not interfere. The normal range is 40-60 U/liter. Lipase activity of pancreatitis patients generally exceed 1000 U/liter during the acute phase and 250 U/liter for as long as 10 days after it.
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PMID:Lipoxygenic micromethod for specific determination of lipase activity in serum and duodenal fluid. 1 45

Pancreatitis developed in 6 patients in the National Cooperative Crohn's Disease Study. In five of these the diagnosis was confirmed by elevated levels of seum amylase or lipase. All cases were in the 113 patients who received azathioprine and occurred within the first 21 days of treatment. This incidence of pancreatitis was significantly greater than in the patients treated with sulfasalazine, prednisone, or placebo (P less than 0.01).
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PMID:Azathioprine-related pancreatitis in patients with Crohn's disease. 3 78

Amylase isoenzyme analysis of serum and urine has been performed in 4001 normal persons and 500 patients with various disease using electrophoresis on thin layer polyacrylamide gel. Although elevation of amylase activity in amylase-1 and 2 has been reported to be the specific findings in patients with pancreatitis, 1.69% of normal persons had an elevated Amylase-2(named "Dominant Amylase-2") up to the same levels as major isoenzymes (Amylase-1 and 3), along with Amylase-1. Pedigree study confirmed an autosomal dominant mode of inheritance for Dominant Amylase-2. Knowledge of the genetic polymorphism is of importance in clinical assessment of amylase isoenzymes in patients having an elevated Amylase-2 suggestive of pancreatitis. Predominance of the pancreatic components in serum and urine has been revealed to be a specific index of pancreatic involvement. However, the existecne of an inherited trait of pancreatitis-like isoamylase pattern in healthy individuals must be borne in mind. On the basis of the present study, it may be concluded that a rise in the pancreatic type isoenzymes may not necessarily indicate underlying pancreatitis, especially in the absence of elevated amylase and lipase levels.
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PMID:Clinical evaluation of the pancreatitis-like isoamylase pattern in normal persons. 15 Sep 92

At first the review deals with significance of the apoproteins for the metabolism of the lipoproteins, especially VLDL. Thus, for instance the apo-C is a cofactor for the lipase of the fatty tissue which hydrolyses the chylomicron-TG. The author enters examples of the secondary hyperlipoproteinaemias: hyperlipoproteinaemias in diseases of the liver and of the kidneys, in pancreatitis and in diabetes. In cholestasis an abnormal lipoprotein called LP-X is observed, in other diseases of the liver the beta2LP corresponding to the VLDL-intermediate. Causes for increases of lipoproteins in renal diseases are probably disturbances of the protein metabolism. There are close correlations between hyperlipoproteinaemias and pancreatitis. In diabetes primary hyperlipoproteinaemias in maturity-onset-diabetes are to be differed from clearly secondary ones in juvenile-onset-diabetes as well as such ones in nephropathy. The therapy of the secondary hyperlipoproteinaemias is shortly discussed.
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PMID:[Secondary hyperlipoproteinemias]. 19 82

An experimental xenogeneic immune pancreatitis was induced in AB-mice by repeated intraperitoneal injections of rabbit immune sera directed against purified pancreatic enzymes (alpha-amylase, lipase, trypsin) for 3 hours up to 8 days. Histologically, the immune pancreatitis is characterized by three different findings: 1. Multiple acinar cell necroses on the 2nd, 3rd and 5th day of immune serum application. 2. A dedifferentiating acinar cell atrophy with development of pseudocanalicular acini on the 5th and 9th day. 3. An increasing interstitial histiolymphoplasmocytic pancreatitis on the 5th and 9th experimental day. Ultrastructurally, the acinar cell necroses proved as the final stage of a step-by-step developing acute lethal cell damage. The dedifferentiating acinar cell atrophy corresponds to a chronic sublethal cell injury with alteration of different cytoplasmic components. The interstitial pancreatitis in immune serum treatment is characterized by differently activated histiocytes and lymphocytes as well as by mature plasma cells. Because of immune histological findings (peri- and intraacinar deposition of rabbit globulin, specific fixation of guinea-pig complement, and appearance of mouse globulin in the mouse exocrine pancreas) and control experiments with rabbit and mouse normal serum as well as with physiological saline, the pathogenesis of the induced xenogeneic immune pancreatitis is regarded as a twophase process: 1. The acinar cell necroses are mainly due to a cytotoxic immune reaction (possibly in combination with an immune complex reaction) caused by specific anti-pancreatic enzyme antibodies of the applied immune sera. The dedifferentiating acinar cell atrophy may be the result of a specific action of the anti-enzyme antibodies against the corresponding pancreatic enzymes in the apical secretion granules of the pancreatic acinar cells. 2. The interstitial histiolymphoplasmocytic pancreatitis is mainly the morphologic substrate of an extravascularly (intraperitoneally) induced serum sickness reaction (immune complex reaction) due to the foreign proteins applied with the xenogeneic immune sera.
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PMID:Experimental immune pancreatitis in the mouse by rabbit immune sera directed against purified enzymes of the exocrine pancreas. 30 66

In 21 female Beagle dogs an experimental pancreatitis was induced by injection of bile into the pancreatic duct system. Beside controls, dogs received 62.5 micrograms/h cyclic somatostatin (SRIF) a continuous i.v. infusion starting with a bolus of 250 micrograms 15 minutes before or 2 hours after bile injection. Following blood parameters were determined: lipase, amylase, blood count, minerals, glucose, insulin, gastrin, secretin and CCK. Two controls died within 24 hours, the others were sacrificed after 48 hours. All pancreata were examined morephologically. The controls developed all clinical signs of acute hemorrhagic pancreatitis, whereas all SRIF-treated dogs were in much better general condition. Lipase and amylase increased in all groups. In the controls insulin, gastrin and secretin remained unchanged and CCK rose slightly. SRIF-treatment diminished insulin, CCK and the test meal-induced increase of secretin. At autopsy the pancreata of the controls were nearly entirely apoplectic. The SRIF-treated dogs showed less damage of the pancreas and no severe hemorrhagic necrosis was noted. The beneficial effect of SRIF cannot only be due to an interaction with intestinal hormones. An additional direct protective effect on the exocrine parenchyma is proposed to exist.
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PMID:Effect of somatostatin on bile-induced acute hemorrhagic pancreatitis in the dog. 39 59

Precise relationships between pancreatic ductal obstruction and pancreatic secretory capacity have not been established. In this study, we describe the quantitative relationships between the lengths of opacified ducts obtained at retrograde pancreatography and the secretory capcity of the gland for volume, bicarbonate, lipase, and trypsin. Forty-five patients (17 with pancreatic cancer, 6 pancreatitis, 5 other malignancies, and 17 nonmalignant, nonpancreatic disease found at laparotomy) were studied with a method of duodenal intubation and perfusion with basal saline perfusion alone or with continuous intravenous infusion of secretin or of cholecystokinin-pancreozymin. Secretory outputs of volume, bicarbonate, and enzymes compared with the length of opacified ducts showed a significant (P less than 0.05) linear relationship for patients with pancreatic cancer, pancreatitis, and other cancers. The resulting data imply that obstruction of the pancreatic duct is important in decreasing secretion of the pancreas in pancreatic disease. The relationship between obstruction and pancreatic secretion demonstrates that a decrease in exocrine pancreatic secretion cannot be detected until more than 60% of the total length of the main pancreatic duct has been obstructed.
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PMID:The relationships between pancreatic ductal obstruction and pancreatic secretion in man. 43 Nov 21

A prospective study was conducted on 17 cases of acute pancreatitis; encephalopathy was discovered in six patients (35%). The following parameters were studied: the usual ones in pancreatitis conditions (amylasemia, lipasemia, amylasuria, ions, glucose, pO2, pCO2, pH, etc.), and electroencephalographic changes and determinations in CSF of cells, proteins, lipase, amylase, lipides and cholesterol. A direct relationship was found to exist between the pancreatic encephalopahy condition and an increase in CSF-lipase. The electroencephalographic changes were nonspecific. The encephalopathy did not affect the course of the pancreatitis condition, and showed no relationship to type of treatment involved. The severity of the pancreatitis was not related to the presence or absence of encephalopathy.
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PMID:Pancreatic encephalopathy. 45 37

Uremia results in complex metabolic disturbances of exocrine pancreatic function which increase with the severity of renal insufficiency. This uremic pancreopathy is not identical with the pancreatitis of classical type. Its important clinical indicator is an elevation of serum lipase activity (more than 60% in nondialyzed renal insufficiency; hyperlipasemia was also detectable in chronic hemodialyzed patients (45%). The pathogenesis is heterogenous, its concept based on clinical and experimental studies involves several components: hormonal alterations (calcitonin etc.), catabolic protein metabolism in uremia, systemic disturbances (hemodynamics, hypoxia, acidosis etc.), direct impairment of the pancreatic cells induced by uremic toxins.
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PMID:[Uremic pancreopathy. Clinical and experimental studies of its pathogenesis]. 45 76

We have developed a model of experimental haemorrhagic pancreatitis in pigs with a 100% mortality within 24 h without treatment. In this model we have studied the production of peritioneal exudate and compared the concentrations of amylase, lipase and phospholipase A2 in the ascitic exudate and serum. The results suggest that the determination of phospholipase A2 might be important in the diagnosis and follow-up of acute pancreatitis.
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PMID:Phospholipase A2 in serum and ascitic exudate in experimental acute haemorrhagic pancreatitis in pigs. 51 Mar 26


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