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)

A specific and sensitive radioimmunoassay (R.I.A.) has been developed which makes possible the determination of serum or plasma trypsin concentrations despite the presence of trypsin inhibitors, which have invaldiated previously available enzymatic techniques. The assay was most precise at about 300 microng trypsin standard Ag5 per litre of serum, a value comparable with the mean in 76 healthy volunteers (273 microng/1) and in 20 hospital patients with non-pancreatic disease (266 microng/1). Markedly raised concentrations (970-6500 microng/1) were found in all 14 patients with acute pancreatitis and in 8 patients with chronic renal failure (580-1360 microng/1). Abnormal concentrations were found in 11 of 16 patients (69%) with pancreatic cancer (8 high, 3 low) and in 15 of 23 patients (65%) with chronic pancreatitis (3 high, 12 low). Patients with jaundice had normal or marginally lower than normal concentrations unless pancreatic disease or common-duct gallstones were present.
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PMID:Diagnostic importance of changes in circulating concentrations of immunoreactive trypsin. 6 50

The changes in serum trypsin concentration have been measured in 47 subjects for up to 2 hours after a Lundh meal. In 18 healthy controls, mean fasting trypsin concentration was 285 +/- 125 ng/ml (mean +/- 2 SD). The maximum increase after the Lundh meal (the trypsin response ratio) was 6.7 +/- 7.5%. Six patients with chronic renal failure had elevated fasting serum trypsin concentrations (range 460-1100 ng/ml) but trypsin response ratios fell within the control range. Of five patients with relapsing pancreatitis, two had raised and three normal or low fasting trypsins. After stimulation two had elevated trypsin response ratios; one of the two had evidence of main duct obstruction. Eleven out of 12 patients with chronic pancreatitis (with or without insufficiency) had low fasting trypsin concentrations (range 0-120 ng/ml) Seven of the 12 also had raised trypsin response ratios. In six patients with cancer of the pancreas, fasting trypsin was low in three, normal in two, and raised in one. Both patients with a normal fasting level had a raised trypsin response ratio. The combination of a single estimation of fasting serum trypsin concentration followed by serial measurements after a Lundh meal provides a useful screening test for chronic pancreatic disease.
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PMID:Serum immunoreactive trypsin concentration after a Lundh meal. Its value in the diagnosis of pancreatic disease. 52 92

Plasma immunoreactive glucagon (IRG) concentrations were measured in 36 patients with chronic renal failure (CRF) and 32 normal subjects. In addition, the components of circulating IRG were analyzed by gel filtration in the fasting state and after physiological stimuli. Fasting IRG was elevated (P less than 0.001) in CRF patients (534 +/- 32 pg/ml) compared with the levels found in healthy subjects (113 +/- 9 pg/ml). Oral glucose suppressed plasma IRG in CRF patients from a basal level of 568 +/- 52 to a nadir of 354 +/- 57 pg/ml (120 min). This degree of suppression (38%) was comparable to that found in normal subjects (basal = 154 +/- 20 to 100 +/- 23 pg/ml) at 120 min (35%). Intravenous infusion of arginine (250 mg/kg) resulted in a 71% rise in IRG in CRF patients and a 166% increase in normal subjects. Gel filtration of fasting plasma from CRF patients showed three major peaks. The earliest (A) was found in the void volume (mol wt greater than 40,000) and constituted 16.5 +/- 4.7% of the elution profile. The middle peak (B) eluted just beyond the proinsulin marker (approximately 9,000 mol wt) and constituted the largest proportion of the elution profile (56.5 +/- 3.4%). The third peak (C) coincided with the standard glucagon and [125I]glucagon markers (3,485 mol wt) and comprised 27.0 +/- 4% of the IRG profile. In contrast, only peaks A and C were found in fasting plasma of normal subjects (53.6 +/- 10.4% in A and 46.4 +/- 10.4 in C). After oral glucose, glucagon immunoreactivity in the 3,500 mol wt peak (C) was markedly suppressed, while the B peak in patients with CRF declined to a lesser extent. The A peak in both groups was unchanged. After an arginine infusion only the C peak increased in both groups of subjects. Gel filtration of plasma in 3 M acetic acid gave similar profiles to those obtained in glycine albumin buffer. Exposure of serum to trypsin indicated that the B and C peaks were digestible, while the A peak was resistant to the action of the enzyme. In one sample, peak C increased after a 2-h exposure of serum to trypsin. We conclude that circulating IRG in normal subjects and patients with CRF is heterogenous. The hyperglucagonemia of renal failure is largely due to an increase in IRG material of approximately 9,000 mol wt, consistent with proglucagon, although the 3,500 mol wt component is also considerably elevated (threefold). The significance of circulating IRG levels should be interpreted with caution until the relative biological activity of the three components is established.
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PMID:Heterogeneity of plasma glucagon. Circulating components in normal subjects and patients with chronic renal failure. 95 99

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

The frequency and degree of elevated serum levels of trypsin (T) and correlation with other pancreatic enzymes were determined in several groups of patients with renal disease, i.e., patients with chronic renal failure (CRF), hemodialysis patients (HD), renal transplant recipients (RT), and in a control (C) group. Mean values of T were significantly higher in all other groups than in the C group (p less than 0.0001). A statistically significant correlation between T and creatininemia levels was found only for the RT group (p less than 0.0001). Correlations between T versus pancreatic amylase and T versus lipase activity were found to be statistically significant in the CRF and RT groups (p less than 0.01), but not in the HD group. Most patients in all groups had T values higher than the maximum value observed in the controls and, of them, most had very elevated values. The results suggest that in chronic renal pathology there are frequent and significant increases in serum T levels, circulating in parallel with the other pancreatic enzymes. It is possible that, together with the renal excretion impairment, there could also be subclinical pancreatic damage or a dysfunction of the other means of elimination of T that can be responsible for, or contribute to, the serum increase in the enzyme.
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PMID:Serum trypsin in chronic renal failure and transplant patients. 138 54

We studied urinary excretion of active and inactive kallikrein every day for 3 weeks in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) subjected to 5/6 nephrectomy (5/6), 1/2-nephrectomy (1/2) or sham-operation (Sham). We determined urinary active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). In the SHR group, blood pressure was significantly elevated in 5/6-animals as compared with 1/2 or sham, whereas in the WKY group blood pressure was not changed after either operation. Urinary active and total kallikrein excretion were decreased in 5/6-SHR to 34% and 59%, respectively, as compared with values of sham-SHR, and in 1/2-SHR to 70% and 70%, respectively. Similarly, they were also decreased in 5/6-WKY to 36% and 55%, respectively, as compared with values of sham-WKY. In 1/2-WKY urinary active kallikrein excretion was decreased to 88% as compared with the value of sham-WKY, but urinary total kallikrein excretion was not different from that of sham-WKY. Thus, the suppressed renal kallikrein activity due to reduced renal mass was not associated with any significant change in blood pressure in WKY, although it induced an elevation of blood pressure in SHR. These results indicate that the decreased production of renal active kallikrein may not play a significant role in the regulation of blood pressure in the rat remnant kidney model of chronic renal failure. In addition, it is suggested that the elevation of blood pressure in this model of SHR may be due to other factors than renal kallikrein.
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PMID:Role of renal kallikrein in the regulation of blood pressure in the rat remnant kidney model of chronic renal failure. 261 50

To assess the potential role of renal kallikrein-kinin system in enhancing sodium excretion per nephron in chronic renal failure, we studied urinary excretion of active and inactive kallikrein for 3 weeks in Wistar-Kyoto rats subjected to 5/6 nephrectomy (5/6), 1/2 nephrectomy (1/2) or sham operation (Sham). We determined urinary active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). Fractional sodium excretion was significantly increased in 5/6-rats as compared with 1/2- or sham-rats. On the contrary, urinary active kallikrein excretion per nephron was not different in the three models whereas a significant rise in urinary inactive kallikrein excretion per nephron was found in 5/6-rats as compared with 1/2- or sham-rats. Urinary total kallikrein excretion per nephron was significantly increased in 5/6-rats as compared with sham-rats. In addition, no correlation was found between fractional sodium excretion and urinary active kallikrein excretion corrected for creatinine clearance (Ccr) in 5/6-rats. These results indicate that decreased excretion of renal active kallikrein may not play a significant role in the increased sodium excretion per nephron in the rat remnant kidney model of chronic renal failure. Furthermore, it is suggested that in this model of rat there might be impaired production of renal active kallikrein although its exact mechanism remains to be determined.
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PMID:Role of renal kallikrein in the increased fractional sodium excretion in the rat remnant kidney model of chronic renal failure. 261 88

Urinary trypsin inhibitory capacity is mainly due to the excretion of a glycoprotein which is immunologically related to the inter alpha-trypsin inhibitor and may be a proteolytic degradation product of that substance. It was tested in 133 subjects divided into 7 groups: 24 healthy controls (group A), 21 patients with bacterial infection (group B), 37 with bacterial infection under antibiotic therapy (group C), 25 with connective tissue disease (group D), 8 with infected connective tissue disease (group E), 14 with cancer (group F) and 4 with infected cancer (group G). Urinary trypsin inhibitory capacity level was very low in controls (3.32 +/- 0.8 U/g urinary creatinine), but it was dramatically increased when infection was present (149.67 +/- 23.6 U/g urinary creatinine). This test appeared to be more effective than serum C-protein measurement simultaneous carried out in the same patients. Urinary trypsin inhibitory capacity is not related to the degree of proteinuria in the urine sample, but it is increased in patients with chronic renal failure excluded from this study. Thus, its measurement is a sensitive, easy and useful test for detecting and monitoring infections. The return to its physiological value is a very good argument in favour of therapeutic effectiveness.
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PMID:[Clinical value of the determination of urinary antitrypsin activity]. 296 52

Active renin (AR) and trypsin-activated inactive renin (IR) were examined in 32 patients with chronic renal failure (CRF). (of these, 25 patients were kept on the programmed hemodialysis) and in 11 normal subjects. As compared with normal subjects, CRF patients manifested a decrease in both AR and IR. A direct correlation was discovered between AR and IR: R = 0.64, P less than 0.01. The simultaneous decrease in IR and AR attests to the impairment of renin synthesis during CRF.
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PMID:[Inactive renin in patients with chronic and terminal renal insufficiency]. 390 87

We have measured plasma N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) and neuraminidase (EC 3.2.1.18) activities as markers of glycosidase activity and immunoreactive trypsin (EC 3.4.21.4) levels as a marker of proteolytic potential in the plasma of normal and uraemic subjects. The levels of all of these enzymes are significantly elevated in the plasma of uraemic subjects when compared to normal. We have postulated that the combined attack of glycosidases and proteases on erythropoietin will lead to fragmentation of this glycoprotein hormone with loss of activity. This may be a major contributory cause to the anaemia of chronic renal failure.
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PMID:Increased plasma glycosidase and protease activity in uraemia: possible role in the aetiology of the anaemia of chronic renal failure. 390 90


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