Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary excretion of alpha-glucosidase (AGL), gamma-glutamyltransferase (GGT) and ribonuclease (RNase), and serum amylase and immunoreactive trypsin (IRT) were determined in 38 control subjects, 48 patients with pancreatic cancer, 77 with chronic pancreatitis and 47 with extrapancreatic diseases in order to ascertain the presence of a renal tubular damage and to investigate its etiology. A significantly increased frequency of pathological results for all urinary enzymes was documented in the various groups of patients as compared to controls. Significant correlations were detected among AGL, GGT and RNase. Considering the subjects as a whole, GGT and RNase excretions correlated with serum IRT and amylase; the two urinary enzymes were found to be higher when jaundice was present. In chronic pancreatic disease enzymuria was related to increased serum pancreatic enzymes; in extrapancreatic diseases it was associated to hyperbilirubinemia. The vast majority of patients with pancreatic cancer and elevated urinary enzymes presented hepatic metastases and/or jaundice. We can conclude that an anatomical and functional tubular impairment is detectable in some patients with chronic pancreatic and extrapancreatic diseases. Tubular damage seems to least in part to be related to pancreatic inflammation and necrosis in chronic pancreatic disease, while jaundice may be found to play an important role in diseases of the hepatobiliary tract. In pancreatic cancer, liver dysfunction (presence of liver metastases and/or extrahepatic cholestasis) also appears to be involved in altering tubular cells.
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PMID:Renal tubular dysfunction in pancreatic cancer and chronic pancreatitis. 256 74

Serum and urine elastase 1, its renal output and clearance and urinary gamma-glutamyltransferase and ribonuclease excretions were measured in 16 patients with pancreatic cancer, 23 with chronic pancreatitis and in 22 healthy controls in order to evaluate elastase 1 plasma-urine transfer in chronic pancreatic disease and to investigate any factors that might influence the clearance of this enzyme. In an additional group of 17 patients with different pancreatic diseases the serum molecular size distribution of elastase 1 after chromatography was ascertained. An increased urinary elastase 1 output was found in 4/16 patients with pancreatic cancer and in 6/23 with chronic pancreatitis. No correlation was found between circulating elastase 1 and its urinary output; a negative correlation was detected between the serum levels of this enzyme and its clearance. The excretion of ribonuclease and gamma-glutamyltransferase was correlated with elastase 1 output and clearance. While the majority of elastase 1 in serum was accounted for by high molecular forms, probably the expression of complexes with serum inhibitors, free circulating enzyme was present in all patients with high serum elastase 1. Our findings suggest that elastase 1 urinary excretion increases in some patients with chronic pancreatic disease regardless of the neoplastic or inflammatory nature of the illness. Although the availability of different amounts of ultrafiltrable enzyme may play a role in influencing elastase 1 plasma-urine transfer, renal tubular damage appears to be the most important factor influencing the increase in the urinary output of elastase 1.
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PMID:Urinary elastase 1 in chronic pancreatic disease. 259 50

In order to investigate the role of circulating free trypsinogen and renal tubular dysfunction in affecting trypsin plasma-urine transfer, serum immunoreactive trypsin (IRT), its urinary output, IRT molecular size distribution, filtrable immunoreactive trypsin, gamma-glutamyltransferase and alpha-glucosidase outputs were studied in 6 control subjects, 9 patients with pancreatic cancer and 15 with chronic pancreatitis. The majority of immunoreactivity was always eluted at a molecular weight of about 24,000 and might therefore be considered as free trypsinogen. Variable amounts of IRT at higher molecular weights, possibly represented by trypsin-inhibitor complexes, were also detected. Increasing IRT levels were generally accounted for by free trypsinogen, regardless of the nature of the disease. Unlike serum free trypsinogen levels, renal tubular damage, evaluated by means of the excretion of two high-molecular weight urinary enzymes, seems to play a prominent role in explaining trypsin plasma-urine transfer.
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PMID:Molecular size distribution of immunoreactive trypsin and renal tubular dysfunction: role in trypsin plasma-urine transfer. 288 33

In order to investigate the role of renal factors in affecting trypsinogen 1 metabolism and excretion in chronic pancreatic disease, serum immunoreactive trypsin (IRT), urinary IRT, gamma-glutamyltransferase (GGT), alpha-glucosidase (AGL) and RNase outputs and the molecular size distribution of serum and urine IRT were studied in 8 control subjects, 18 cases with pancreatic cancer, and 23 cases with chronic pancreatitis. Serum chromatography demonstrated that most immunoreactivity eluted as trypsinogen 1. Smaller amounts of immunoreactivity at higher molecular weights were also observed. Urine chromatography displayed both trypsinogen 1 and heavier molecular forms. An inverse linear correlation was noticed between creatinine clearance and serum trypsinogen 1 levels. Multiple regression analysis (urinary IRT output dependent and GGT, AGL, and RNase predictor variables) showed a significant linear correlation. RNase was found to be the most important parameter in explaining urinary IRT output. Mild variations in the glomerular function seem to be able to influence serum trypsinogen 1 levels. Urinary IRT excretion is principally explained by a disturbance in the tubular reabsorption of low molecular weight proteins, such as RNase.
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PMID:Renal factors in serum trypsinogen 1 metabolism and excretion in chronic pancreatic disease. 336 41

Pancreatic juice gamma-glutamyltransferase (GGT, EC 2.3.2.2) has been proposed as a marker of pancreatic disease. We have collected pancreatic juice endoscopically from 24 control patients and 43 patients with a variety of hepatic, pancreatic, and biliary disorders. Pancreatic juice GGT, alanine transaminase (ALT, EC 2.6.1.2), and alkaline phosphatase (ALP, EC 3.1.3.1) were measured and found to be present in all samples. GGT was significantly higher in patients with pancreatic cancer (range 21-1175 IU/liter, P less than 0.005) compared with controls (range 2-52 IU/liter). Of 17 patients with pancreatic juice GGT concentrations greater than 52 IU/liter, eleven had definite pancreatic disease (seven pancreatic cancer, four chronic pancreatitis) and, in the remaining six, pancreatitis was possible although not proven. Pancreatic juice ALT and ALP provided no useful diagnostic criteria. GGT in pancreatic juice seems to be a nonspecific marker of pancreatic disease and merits further study.
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PMID:Pancreatic juice gamma-glutamyltransferase, alanine transaminase, and alkaline phosphatase in pancreatic disease. 610 99

A 15-year-old boy with a medical background of obesity, familial hyperlipidemia and acute recurrent pancreatitis, presented to emergency department reporting a 3-day course of periumbilical abdominal pain and nausea. Pain was noticed on epigastric palpation. Laboratory evaluation revealed leucocytosis, neutrophilia and pancreatic enzymes elevation more than three times the upper limit of normal. An acute recurrence of pancreatitis was diagnosed, was admitted to the hospital, being discharged after 5 days. Four days after, he was readmitted because of symptoms recurrence. Elevation of transaminases, gamma-glutamyltransferase (GGT) and direct bilirubin were noticed. Pancreatic enzymes still elevated but lower than in the previous episode. An endoscopic ultrasound revealed a Wirsung with a cephalic stricture and diffuse structural abnormalities suggestive of chronic pancreatitis. The patients was submitted to endotherapy with several sessions of endoscopic retrograde cholangiopancreatography including stenting and pancreatoscopy with marked clinical and imaging improvement. A genetic variant was identified.
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PMID:Chronic pancreatitis in children: treat like an adult? 3175 27