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)

Pure pancreatic juice was collected from 8 control subjects, 12 patients with chronic pancreatitis and 4 patients with cancer of the pancreas by endoscopic retrograde cannulation of the papilla. Samples were collected at 1 minute intervals for 20 minutes after rapid intravenous injection of secretin (Eisai, 1 U/kg) and for 10 minutes after rapid intravenous injection of CCK-PZ (Boots, 1 U/kg). Determinations of volume, bicarbonate concentration and three hydrolases (amylase, chymotrypsinogen and lipase) were made. Our tentative conclusions are (1) pancreatic enzymes are likely to be affected one after another, not in parallel fashing, in chronic pancreatitis and in cancer of the pancreas, (2) bicarbonate concentration and chymotrypsinogen or lipase are most susceptible in chronic pancreatitis and lipase secretion seems to be more susceptible than other parameters in cancer of the pancreas. Amylase is the least affected enzyme in both pancreatic diseases, and (3) determinations of chymotrypsinogen and/or lipase should be preferably performed among hydrolytic enzymes in the evaluation of exocrine pancreatic function in chronic pancreatitis and cancer of the pancreas.
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PMID:Analysis of human pure pancreatic juice in chronic pancreatitis and cancer of the pancreas. 74 91

Endoscopic retrograde pancreaticography (ERP) and secretin-pancreozymin test corrected for losses (SP test) were performed in 153 patients suspected to have pancreatic disorders in order to evaluate diagnostic significance of these procedures. Pancreatic sonography was done in addition in 110 of these patients. If pancreatic excretion was normal, ERP results turned out to be normal in the same patients as well. SP test involves rather extensive laboratory work-up, but it does yield the most precise results as far as diagnosis of chronic pancreatitis is concerned. For this reason, and because of the possible complications caused by ERP, ERP should be applied only, when surgery is considered. Results of SP test and sonography coincided rather well. Therefore, sonography, not doing any harm to the patient, does have its place in the diagnosis of chronic pancreatitis.
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PMID:[Chronic pancreatitis: diagnostic value of endoscopic retrograde pancreaticography, of pancreatic sonography, and of secretin-pancreozymin test corrected for volume losses (author's transl)]. 76 59

Calcium enters the pancreatic juice from two sources, one fraction associated with enzyme protein and another small fraction presumably by diffusion. The calcium concentration in pancreatic juice is lower than in plasma. It decreases with high flow rates and increases asymptotically to plasma concentration with low rates. In chronic pancreatitis calcium concentration is raised in the secretin-stimulated juice. After pancreozymin in moderate chronic pancreatitis it is low but in severe stages of the disease it is high signalling total dissociation from the entrance of enzyme protein, which is very low in these cases. Hypercalcemia stimulates enzyme secretion in the pancreas, hypocalcemia inhibits it. Calcium is essential for intracellular processes associated with secretion, the exact place in the sequence of "stimulus-secretion-coupling" still being unknown. Calcitonin as one of the hormones which regulates calcium homeostasis, inhibits secretion of enzymes but not of fluid and bicarbonate. The action of the parathyroid hormone on the exocrine pancreas is unknown. In primary hyperparathyroidism with chronic hypercalcemia acute and chronic pancreatitis occur 10 to 20 times more frequently than in the general population. In acute pancreatitis of whatever origin hypocalcemia is atypical feature of the disease indicating bad prognosis. The mechanism of its development is still unclear. In chronic pancreatitis the forming of calcified stones in the ducts is typical in cases associated with alcoholism, with protein malnutrition and with primary hyperparathyroidism. But it occurs also in cases with unknown etiology signalling a more general pathophysiological phenomenon. The calcium salts form a precipitate on protein plugs in the juice, which have been observed even in early stages of the disease in the small and larger ducts of the gland.
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PMID:The role of calcium in pancreatic secretion and disease. 77 77

The prevalence of diabetes due to chronic pancreatitis would appear to be increasing. In western countries this is associated with the known increase in alcohol consumption and AIP. Malnutrition may be etiologic in tropical areas. The incidence of diabetes in chronic pancreatitis is dependent on a number of factors. It is more common in alcohol-induced pancreatitis, rarely occurs after the first attack but tends to increase with time and rises markedly in calcific pancreatitis. Abnormal glucose tolerance occurred in 91% of patients with calcific pancreatitis and 70% of patients with noncalific AIP in our follow up of five to 12 years. This stresses the importance of serial regular glucose tolerance tests in these patients (Table I). The insulin-reserve is severely depleted in most patients who do not yet demonstrate abnormal glucose tolerance, indicating that pancreatitis regularly affects the islets and that nearly all patients are potential diabetics. The beta cells appear to respond better to oral glucose, glucagon or secretin than to i.v. glucose suggesting a selective glucose receptor loss or block to hyperglycemia in chronic pancreatitis. The alpha cells seem to be more resistant to the effects of chronic pancreatitis but true hypoglucagonemia was found in 16% of patients. In addition, stimulated growth hormone secretion may be deficient in pancreatic diabetes. These last two factors, among others, may be responsible for the protracted and even fatal hypoglycemia to which some patients with AIP on insulin therapy are liable. The danger of drug-induced hypoglycemia, coupled with the infrequency of vasculopathy, retinopathy and nephropathy in pancreatic diabetes has induced us to keep these patients hyperglycemic and glycosuric rather than in a sugar-free state, as long as symptoms are contained. Recurrent abdominal pain, marked weight loss and associated steatorrhea often raise special problems in the management of the pancreatic diabetic.
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PMID:Clinical and hormonal aspects of pancreatic diabetes. 80 21

The response of the pancreas to standard (1.0 U/kg) and augmented (4.0-5.0 U/kg) doses of secretin was compared in normal subjects and patients. The results of the investigation showed that for clinical purposes the standard test is sufficient for the diagnosis of pancreatic diseases causing gross destruction of the parenchyma. The augmented test is of particular value when the response to 1 U/kg produces equivocal results, since greater stimulation enhances the masked secretory deficiency. The effect of the augmented stimulus in alcoholic patients suggests the hypothesis that the post-secretin response pattern of minimal pancreatic inflammatory disease is hypersecretion. Repeated observation is alcoholic hypersecretors has provided data which can explain the evolution of pancreatic pathology in the terminal stages of chronic pancreatitis.
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PMID:[Standard and Augmented Secretin Tests in Chronic Pancreatitis]. 81 72

The concentration of calcium in the pancreatic juice is lower than in plasma. Two calcium fractions occur in the juice, the one associated with the enzyme protein and the other entering the juice via diffusion. In chronic pancreatitis the calcium concentration of the juice is increased in post-secretin periods. Hypercalcemia stimulates enzyme secretion and elevates calcium concentration in the juice. Hypocalcemia inhibits secretion of enzymes and fluid. Calcium is an important mediator substance for the secretion of pancreatic hydrolases at the intracellular level. In primary hyperparathyroidism with chronic hypercalcemia the prevalence of acute and chronic pancreatitis is 10--12 times higher than in normal population. In chronic pancreatitis caused by alcoholism, primary hyperparathyroidism, and chronic protein deficiency without alcoholism calcifying duct stones are seen in the pancreas in high frequency.
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PMID:[Calcium, pancreatic secretion and pancreatitis (author's transl)]. 82 62

The pancreatic excretion test with a weak acid of 5, 5-dimethyl-2,4-oxazolidinedione (DMO) was performed concomitantly with the pancreozymin-secretin test in 28 patients with pancreatolithiasis, 14 patients with pancreatic carcinoma, and 67 healthy subjects. The DMO concentration and total output of duodenal content after secretin stimulation, when corrected to the simultaneously determined plasma DMO concentration, were significantly reduced in the patients. While the pancreozymin-secretin test was abnormal in 96% of patients with pancreatolithiasis and in 86% of those with pancreatic carcinoma, the pancreatic DMO excretion test gave abnormal results in 100% of the patients. This suggests that the new test may well become effective in detecting early stages of pancreatic disease including carcinoma and chronic pancreatitis.
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PMID:Pancreatolithiasis and pancreatic carcinoma. Evaluation of pancreatic excretion test with 5,5-dimethyl-2,4-oxazolidinedione. 86 46

The CEA concentration in duodenal fluid after secretin-CCK stimulation has been investigated in 16 patients with pancreatic disease (6 with pancreatic carcinoma and 10 with chronic pancreatitis), 9 with non-pancreatic disease, and 10 control subjects. The purpose was to study whether the determination of CEA in duodenal fluid during the secretin-CCK test can give any additional information for the diagnosis of pancreatic disease and for differentiation between pancreatitis and carcinoma. We found that high values of CEA in duodenal fluid do not necessarily indicate pancreatic carcinoma. Moreover, the level may be elevated in non-pancreatic disease.
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PMID:The CEA concentration in duodenal fluid in patients with pancreatic disease. 92 16

Exocrine pancreatic function has been evaluated in 24 controls and 29 patients with confirmed chronic pancreatitis by continuous infusion (90 min) of synthetic caerulein, 100 ng/kg/h, plus GIH secretin, 1 CU/kg/h. Mean secretory values of the controls were comparable to those obtained by others using maximal doses of secretin and CCK. Unlike the controls, patients suffering from chronic pancreatitis demonstrated a progressive reduction in secretion during infusion. Thus, the comparison of responses for the final 30-min period gave much clearer and more complete discrimination between normal and abnormal pancreatic function than the preceding 30-min period.
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PMID:Investigation of exocrine pancreatic function by continuous infusion of caerulein and secretin in normal subjects and in chronic pancreatitis. 95 84

In order to study whether or not mucosubstance increases occur in the pancreatic juice of patients with chronic pancreatitis, hexosamine was measured in duodenal aspirates during the secretin phase (S-40) following pancreozymin-secretin stimulation in 16 normal subjects, 37 patients with chronic pancreatitis, 6 patients with alcoholism, 13 patients with gallstones, and 11 patients with peptic ulcer. The hexosamine concentrations in the pancreatic secretions showed a negative correlation with the bicarbonate concentrations and volume output. Rises in hexosamine concentration were seen in alcoholism and chronic pancreatitis, especially in alcoholic pancreatitis. This is probably intimately related with the repeated ingestion of large amounts of alcohol over long periods of time. Since high hexosamine values are noted in the relapsing type of chronic alcoholic pancreatitis, increases in viscosity due to mucosubstance increases in the pancreatic juice are probably related with the recurrence of acute attacks accompanying ductal stenosis or obstruction.
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PMID:The behavior of mucopolysaccharide in the pancreatic juice in chronic pancreatitis. 95 74


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