Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic function tests were performed in 15 patients with advanced renal insufficiency. Pancreatic secretion was stimulated with CCK/PZ and secretin and 60 minutes later with bile given intraduodenally and CCK/PZ and secretin intravenously. The Wilcoxon-test showed that there were significantly higher lipase levels in serum and lower amylase amounts in duodenal juice compared to normal volunteers. No differences could be demonstratd for volume, maximal bicarbonate concentration, lipase and trypsin outputs. It could be shown by nonlinear discriminant analysis that pancreatic secretion might specifically be changed in patients with chronic renal failure. These patients can be definitely differentiated according to the secretion pattern from normal controls and patients with chronic pancreatitis, pancreatic carcinoma, chronic and acute duodenal ulcer.
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PMID:[Pancreatic secretion of patients with chronic renal insufficiency (author's transl)]. 114 6

Amylase concentration in serum is frequently found increased in chronic renal insufficiency without being associated with pancreatic diseases. A prospective study was performed in 71 patients with chronic renal insufficiency undergoing hemodialysis for comparison of different pancreatic enzymes in serum. 7 patients were not considered in this comparative study because of chronic pancreatitis-like-changes in ultrasound. Increased serum concentrations were found for total amylase in 27 patients (42.2%), pancreatic amylase in 26 patients (25.0%), lipase in 50 patients (78.1%), immunoreactive trypsin in 61 patients (95.3%) and for elastase 1 in 7 patients (10.9%). Hemodialysis did not affect any of the investigated pancreatic serum-enzymes. Elastase 1 determination in serum appears superior to the other pancreatic serum-enzymes because of higher specificity, not limited by renal insufficiency. The different serum concentration of elastase 1 and trypsin, which have a similar molecular weight, points towards a completely different clearance mechanism for these enzymes.
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PMID:[Effect of chronic renal failure and hemodialysis on the pancreas-specific enzyme pattern in the serum]. 169 2

Results vary with regard to the upper limits of serum amylase seen in patients with renal failure, and very little has been reported with patients with renal insufficiency not yet requiring dialysis. To determine the level of serum amylase elevation in renal insufficiency and renal failure, we determined serum amylase values in 128 subjects with creatinine clearances less than 90 ml/min. Serum amylase remained in the normal range when creatinine clearance was greater than 50 ml/min, and did not become elevated until creatinine clearance was less than 50 ml/min. The highest serum amylase recorded in the absence of acute pancreatitis was 503 IU/L (normal, less than 128 IU/L). Serum lipase and trypsin values paralleled those for serum amylase; values remained normal when creatinine clearance was greater than 50 ml/min, and were normal or elevated when creatinine clearance was less than 50 ml/min. These results indicate that elevations of serum amylase (i.e., amylase greater than 128 but less than 500 IU/L) in asymptomatic patients with impaired renal function are not evident until creatinine clearances fall below 50 ml/min, and probably do not represent acute pancreatitis.
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PMID:Serum amylase in patients with renal insufficiency and renal failure. 169 13

Serum elastase 1 has been evaluated in 115 patients with pancreatic and nonpancreatic gastrointestinal diseases and in 36 healthy controls. Increased serum elastase 1 values were found in all 27 patients with acute pancreatitis. If the diagnostic cutoff was established as the 2-fold increase above the upper normal range, sensitivity of elastase 1 (100%) was superior to pancreatic lipase (90%), immunoreactive trypsin (87%) and pancreatic amylase (78%). Specificity was 96% for elastase 1 at this cutoff. No distinction was possible between edematous and necrotizing acute pancreatitis on the basis of peak serum elastase 1 concentrations. Among 32 patients with chronic pancreatitis increased serum elastase 1 values were found in 22% and decreased values in 16% of patients, showing a striking parallelism to serum values of pancreatic lipase and immunoreactive trypsin. Specificity, established in controls and 49 patients with different gastrointestinal diseases, was 77% for elastase 1, 76% for immunoreactive trypsin, 83% for pancreatic lipase and 91% for pancreatic amylase. In addition, we investigated 21 patients with severe chronic renal diseases. In patients with renal insufficiency elastase was increased in 33%, comparable to the frequency of increased amylase and pancreatic amylase serum levels, whereas immunoreactive trypsin was increased in 95%. Immunoreactive trypsin showed a significant correlation to creatinin serum concentration, whereas the other enzymes did not.
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PMID:Serum elastase 1 in inflammatory pancreatic and gastrointestinal diseases and in renal insufficiency. A comparison with other serum pancreatic enzymes. 244 75

The action of blood serum from uremic rats and chronically hemodialyzed patients was investigated for effects on alpha 2-adrenoceptors labeled with 3H-clonidine. Compared to blood sera of rats and patients with normal kidney function, uremic serum significantly inhibited specific 3H-clonidine binding. In saturation experiments the density and affinity of alpha 2-adrenoceptors for 3H-clonidine was lowered by uremic serum. Heating, or trypsin or lipase treatment of the serum did not affect this phenomenon. The effect of the patient's serum could likewise be demonstrated after hemodialysis treatment. The presence of an allosteric regulating substance for clonidine binding to adrenoceptors could at least partially explain the altered and attenuated action of this drug in renal insufficiency.
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PMID:Influence of an uremia-associated serum factor on CNS alpha 2-adrenoceptors. 256 Feb 24

To understand the renal microcirculation in acute pancreatitis is important to know the pathophysiology of renal insufficiency frequently observed as one of multiple organ failures in severe acute pancreatitis. In mongrel dogs acute pancreatitis was experimentally introduced by autologous bile added trypsin injection into the pancreatic duct. The effect of new synthesized pancreatic protease inhibitor (PATM) and dopamine in a dose of 3mg/kg/hr and 10 micrograms/kg/min were investigated, respectively. In acute pancreatitis dogs, renal arterial blood flow and renal tissue blood flow immediately fell and gradually decreased in time course of experiment and renal vascular resistance increased from 2 hours after onset of pancreatitis. When pancreatic protease inhibitor (PATM) was infused in acute pancreatitis dogs, blood pressure and pulse pressure relatively preserved during the experiment. Renal blood flow and renal tissue blood flow were maintained during the first 1 hour and thereafter slightly decreased, however which was less than that of no PATM treated dogs. When dopamine was infused in acute pancreatitis dogs, blood pressure was maintained during the first 90 minutes thereafter remarkably decreased. Renal blood flow was maintained within 60 minutes, however it remarkably decreased at the end of the experiment. This study suggested that renal microcirculation was disturbed from early period of acute pancreatitis in dogs and pancreatic protease inhibitor (PATM) had a beneficial effect of maintain the renal microcirculation.
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PMID:[Renal microcirculation in experimental acute pancreatitis of dogs--the effect of pancreatic protease inhibitor and dopamine]. 323 Dec 8

Since one mechanism by which converting enzyme inhibition (CEI) increases renin is removal of angiotensin II negative feedback on the juxtaglomerular cell, we studied the time course of changes in active and inactive renin after CEI. After equilibration on a 25 meq/day sodium diet, captopril was given as a single 50-mg oral dose (acute phase), and then was administered as 50 mg every 6 h for 3 days to seven normal volunteers (chronic phase). In the acute phase, supine blood pressure fell 12 +/- 2 mm Hg (P less than 0.02). Active renin acutely increased 12.5 +/- 0.9 times the baseline value, peaking at 3-4 h. Inactive renin, measured by acid activation of trypsin activation, decreased in all subjects to 10% or less of control from 2 to as long as 6 h post-CEI and then returned to baseline levels by 8 h (P less than 0.01). With chronic CEI, active renin was elevated to 10.8 +/- 2.4 times the baseline level, and after 48 h inactive renin levels rose to 4.0 +/- 0.6 times the baseline (P less than 0.02). To determine whether the acute changes in inactive and active renin occurred because of captopril's effect on renin in the circulation or kidney, a single dose of captopril was administered to three subjects with mild to moderate renal insufficiency and hyporeninemic hypoaldosteronism. In contrast to normal subjects, these patients had no change in active and inactive renin levels when given captopril, suggesting that changes observed in the normals were renal mediated rather than a plasma phenomenon. We conclude that CEI 1) acutely increases active renin while reciprocally reducing the inactive form, and 2) chronically increases both active and inactive renin. These studies support the hypothesis that inactive renin may be a precursor of circulating active renin.
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PMID:Reciprocal changes in active and inactive renin after converting enzyme inhibition in normal man. 629 83

Patients with chronic renal failure have an abnormal immunoreactive gastrointestinal hormone profile, which is characterised by raised fasting serum concentrations of hormones that have antagonistic effects on exocrine pancreatic function. In addition, in this present study we have found that in renal insufficiency cholecystokinin disappears slowly from the plasma after a constant intravenous infusion of the hormone (p = 0.05 compared with healthy subjects). To evaluate whether the stimulatory or inhibitory hormones have a predominant effect, pancreatic exocrine function under conditions of mannitol perfusion of the duodenum and continuous intravenous cholecystokinin stimulation was studied in eight patients who had severe chronic renal failure and eight age-matched and sex-matched control subjects. Compared with healthy subjects, patients with renal insufficiency had hypersecretion of trypsin in response both to mannitol perfusion of the duodenum and to cholecystokinin stimulation (p less than 0.05). No significant differences in lipase secretion were noted between the patients with renal insufficiency and control subjects. These findings are consistent with the hypothesis that, of the abnormally raised fasting serum concentrations of gastrointestinal hormones found in renal insufficiency, hormones that stimulate rather than inhibit pancreatic exocrine function predominate. Secondly, the dissociation between trypsin and lipase outputs in chronic renal failure may suggest a differential trophic influence of stimulatory hormones -- that is, hypercholecystokininaemia -- on pancreatic exocrine enzyme secretion.
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PMID:Pancreatic exocrine function in severe human chronic renal failure. 680 12

In 121 patients with either liver cirrhosis or chronic renal failure, abnormal values for the concentrations of two pancreatic enzymes in serum were a frequent finding. In renal insufficiency a decreased rate of enzyme elimination is the most likely cause of the above-normal values we observed for serum immunoreactive trypsin and pancreatic isoamylase activity. As for patients with liver cirrhosis, we believe that changes in entrance rates into the blood--i.e., an affected pancreas--is a likely explanation of the abnormally high values we often found for these serum enzymes.
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PMID:Immunoreactive trypsin and pancreatic isoamylase activity in serum of patients with chronic renal failure or hepatic cirrhosis. 697 16

According to the literature, the mean values of immunoreactive serum trypsin (IRT) (RIA-gnost Hoechst) in controls vary considerably between 150 and 283 ng/ml. The reasons for these variations are unknown. The purpose of the present investigation was to study the variations of IRT in relation to age in adults. We studied 124 hospital controls, who were without evidence of pancreatic disease or renal insufficiency and who varied in age between 17 and 84 years. Utilizing the kit of Hoechst, IRT was determined in fasting serum specimens. The mean (+/- SD) in patients over 60 years was 469.6 +/- 197.4 ng/ml, in contrast to 309.1 +/- 118.9 ng/ml (30-59 years) and 209.7 +/- 80.7 (less than 30 years). Of cases over 60 years 36.5% had elevated IRT levels above 500 ng/ml. In 25 cases over 60 years no correlation was found between IRT levels and creatinine clearance and in eight of ten cases of this group with high IRT (greater than 500 ng/ml) the serum pancreatic isoamylase levels were normal. The data indicate that in the diagnosis of pancreatic disease the higher reference ranges in the elderly people have to be taken into account. The age-related higher reference ranges seem not to be due to subclinical renal disease nor to clinically evident pancreatic disease.
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PMID:Variations with age of immunoreactive serum trypsin: higher reference ranges in "healthy" elderly people. 707 23


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