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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied insulin responses to glucose with and without cholecystokinin-pancreozymin and aminophyllin infusions in normal, chronic pancreatitic and genetic (maturity-onset) diabetic subjects. Glucose was given alone as separate 5 and 10 g boluses followed by infusion at 250 mg/min. and 500 mg/min., respectively. Chronic pancreatitis patients and genetic diabetic patients had decreased Imax values, indicating a decreased insulin reserve. Sensitivity to glucose was normal in pancreatitic subjects, but the diabetic subjects had a raised G50 value, compatible with glucoreceptor dysfunction. Infusions of aminophyllin enhanced insulin responses (Imax) to glucose injection in normal subjects and to a lesser degree in pancreatitic subjects, but decreased sensitivity to glucose (increase in G50) in both groups. Although the Imax value in pancreatitic subjects was significantly lower than in the control subjects during the glucose plus aminophyllin infusion, the blood glucose concentration in the pancreatitic subjects was nonetheless decreased. This suggests that pancreatitic subjects have increased endogenous insulin sensitivity. Aminophyllin had no effect in diabetic subjects. Crude cholecystokinin-pancreozymin changed the shape of the glucose/insulin dose response curve in normal, pancreatitic and diabetic subjects. These findings further suggest that the defect in insulin secretion in pancreatitic subjects is partly situated at the cyclic adenosine monophosphate stage of insulin release. Crude cholecystokin-pancreozymin seems to affect insulin release at a point beyond the cyclic adenosine monophosphate stage.
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PMID:Kinetics of insulin secretion in chronic pancreatitis and mild maturity onset diabetes. (Evidence for "gut hormone" action beyond glucoreceptor and cyclic adenosine monophosphate mediated insulin release). 18 56

Secretin (1 CU/Kg) plus Caerulein (100 ng/Kg) or Cholecystokinin (1 or 2 IvyU/Kg) were given by rapid intravenous injection (Schedule 1) or by continuous infusion (Schedule 2) to 63 control subjects (C) and 69 patients affected by chronic pancreatitis (CP). Duodenal juice was collected for two and four 30-minute periods in schedule 1 and schedule 2, respectively. Volume, bicarbonate, and enzyme content were measured. Secretin-Daerulein, by rapid intravenous injection, showed a strong overlapping between C and CP values and led to some side-effects. Secretin-Caerulein by continuous intravenous infusion gave almost identical results as the Secretin-Cholecystokinin.
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PMID:The role of caerulein in tests of exocrine pancreatic function. 34 11

Plasma CEA concentration before and after administration of secretin and cholecystokinin-pancreozymin has been determined in 89 patients with neoplastic or inflammatory pancreatric disease and other neoplastic and nonneoplastic disorders. The purpose of the study was to expore the specificity and sensitivity of such a provocation tests. Some rise of the plasma CEA concentration after hormonal stimulation could be observed in several patients in the various groups. However, none of the 37 patients with nonpancreatic disease who had a basal CEA concentration of 6 micrograms/l or less had a maximal CEA concentration above 13 micrograms/l after the stimulation whereas 7 out of 31 patients with pancreatic disease (3 with pancreatic carcinoma and 4 with chronic pancreatitis) showed such an elevation of plasma CEA concentration. Thus, the provocation test showed a satisfactory specificity for pancreatic disease but a low sensitivity. It is suggested that the possibility of an effect of physiologically released gastrointestinal hormones should be considered when "unexplained" high CEA values are found in plasma samples from nonfasting patients.
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PMID:Effect of secretin and cholecystokinin-pancreozymin on plasma CEA concentration in patients with pancreatic carcinoma and pancreatitis. 45 30

The relationship between insulin responses to oral glucose and pancreatic exocrine function were examined in 15 patients with chronic pancreatitis. Good correlations were found between the insulin responses and exocrine pancreatic function measured as the concentrations of pancreatic enzymes in duodenal juice after intravenous cholecystokinin-pancreazymin (CCK-PZ). There appears to be a roughly parallel loss of endocrine and exocrine function in the course of chronic pancreatitis.
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PMID:Insulin secretion and pancreatic exocrine function in patients with chronic pancreatitis. 46 44

Sequential changes in pancreatic secretion were evaluated during a 2- to 3-year follow-up study in 8 dogs provided with Thomas gastric and duodenal fistulas. Four animals were given intragastric ethanol (2 g kg-1) daily for 3 years; 4 others served as controls. In alcohol-fed animals: (1) Flow rate and bicarbonate output in response to 1 clinical unit kg-1 hr-1 of secretin were increased at the end of 2 years but not after 1 year of alcohol feeding. (2) At the end of 2 years, the dose-response curve of pancreatic secretion to cholecystokinin was unchanged but the maximal bicarbonate and water secretion in response to high doses of secretin were increased. Modifications (1) and (2) are explained by reduplication of pancreatic ducts secondary to the development of chronic pancreatitis, verified by biopsy. (3) The previous report by our group of an increased cholecystokinin release in the course of chronic alcohol consumption in dogs seems to be attributable to an artefact. This work shows that the pancreatic response to intraduodenal oleic acid is not significantly modifed by 3 years of alcohol feeding.
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PMID:Chronic alcoholism and canine exocrine pancreas secretion. A long term follow-up study. 55 9

A reliable, sensitive, reproducible and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK) has been developed, using rabbit antisera to highly purified porcine hormone. The natural occurring variant of CCK (39-CCK), in which the ordinary CCK is lengthened from its N-terminus by a hexapeptide, labelled with 125J, and repurified by column chromatography on Sephadex G-10 and on SP-Sephadex C-25, was used as tracer. Separation from antibody-bound labelled 39-CCK was carried out using a double antibody procedure. Non-specific interference with the assay system was abolished by ethanol extractions. Highly purified porcine CCK was used as standard. No significant crossreaction was found with gastrin, motilin, vasoactive polypeptide (VIP), gastric inhibitory polypeptide (GIP), natural and synthetic secretin, pancreatic glucagon or insulin. The sensitivity of the assay is approximately 40 pg/ml of test solution. The mean immunoreactive CCK concentration in 45 fasting normal subjects was 222 pg/ml increasing after food ingestion to 480 pg/ml. Somatostatin was able to abolish the stimulated CCK release. Elevated CCK concentrations were found in chronic pancreatitis. Immunohistochemical identification of pancreozymin cells was carried out either in surgical samples or in biopsy material. Approximately 1650 CCK cells per cross-section in the duodenum of humans have been found. The CCK cells usually appeared elongated, oval or pyramidal in shape and were observed to reach the lumen with their apical cell pole.
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PMID:Estimation of cholecystokinin-pancreozymin (CCK) in human plasma and tissue by a specific radioimmunoassay and the immunohistochemical identification of pancreozymin-producing cells in the duodenum of humans. 56 41

Exocrine pancreatic function after secretin and cholecystokinin stimulation was examined in a group of patients with idiopathic necrosis of the femoral head and in a normal control group. The volume output, bicarbonate and amylase concentrations in the patient group were not significantly lower than in the control group. Taken individually, however, 3 out of 8 patients with idiopathic necrosis of the femoral head had abnormal pancreatic function tests. In 4 patients there was a significant alcohol intake, with a history suggestive of acute pancreatitis in 2. This suggests that in some patients chronic pancreatitis may be a factor in the pathogenesis of idiopathic necrosis of the femoral head.
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PMID:Exocrine pancreatic function in patients with idiopathic necrosis of the femoral head. 73 63

Digestive enzymatic activities (disaccharidases, alkaline phosphatase, peptide hydrolases) have been determined in the mucosa of 14 patients with chronic pancreatitis. All had an abnormal secretin-pancreozymin test. Four patients had insulin-dependent diabetes mellitus, four a pathological glucose tolerance test. Nine patients had steatorrhoea. Maltase, sucrase, and alkaline phosphatase activity was significantly elevated in patients with exocrine pancreatic insufficiency, whereas those of lactase, trehalase, and peptide hydrolase were normal. Patients with steatorrhoea had higher maltase and sucrase activity than those without steatorrhoea, whereas decreased glucose tolerance had no effect on brush border enzymatic activity. It is suggested thatdecreased exocrine rather than decreased endocrine pancreatic function is responsible for the increase in intestinal disaccharidase and alkaline phosphatase activity, possible by the influence of pacreatic enzymes on the turnover of brush border enzymes from the luminal side of the mucosal membranes or by direct hormonal stimulation though cholecystokinin.
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PMID:Influence of exocrine and endocrine pancreatic function on intestinal brush border enaymatic activities. 109 2

A variety of receptors on pancreatic acinar and duct cells regulate both pancreatic exocrine secretion and intracellular processes. These receptors are potential sites of action for therapeutic agents in the treatment of pancreatitis. Cholecystokinin (CCK) receptor antagonists, which may reduce the level of metabolic "stress" on acinar cells, have been shown to mitigate the severity of acute pancreatitis in a number of models. Not all studies have shown a benefit, however, and differences may exist between different structural classes of antagonists. Because increased pancreatic stimulation due to loss of feedback inhibition of CCK has been proposed to contribute to the pain of some patients with chronic pancreatitis, CCK receptor antagonists could also be of benefit in this setting. Somatostatin and its analogs diminish pancreatic secretion of water and electrolytes and have been effective in treating pancreatic fistulas and pseudocysts. These agents are also being evaluated for their ability to reduce pain in chronic pancreatitis (perhaps by reducing ductal pressure by diminishing secretory volume) and mitigating the severity of acute pancreatitis (possibly by reducing the metabolic load on acinar cells). Recently described secretin receptor antagonists may also have therapeutic value as a means of selectively inhibiting pancreatic secretion of water and electrolytes.
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PMID:Receptor strategies in pancreatitis. 134 60

We have made a prospective study in alcoholic patients, with and without hepatic cirrhosis, in order to evaluate the presence of modifications in the composition of pancreatic juice (JPP) and in the pancreatogram that allows us to diagnose the existence of chronic pancreatitis associated with alcoholic cirrhosis (CE). The patients where 23 chronic alcoholics, 13 of them with CE and the other 10 with no hepatic injury (AC). In all, an endoscopic retrograde cholangiopancreatography (CPRE) was made and after having obtained a pancreatogram a intravenous infusion of secretin and cholecystokinin was performed. The total volume, the concentrations and the out-puts of bicarbonate, amylase, lipase and total proteins were measured in the pancreatic juice collected during 12 minutes. The pancreatogram was normal in the 92.3% of CE and in all the AC. Patients with CE had similar values of all the evaluated parameters to AC patients. In conclusion, there seems to be a good correlation between the pancreatogram and the analytic study of JPP, because the JPP has no qualitative and quantitative anomalies when the Wirsung duct is normal. In our opinion the study of JPP is not useful in the diagnostic of chronic pancreatitis associated with alcoholic hepatic cirrhosis.
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PMID:[Pancreatic function and morphology in chronic alcoholism with and without cirrhosis]. 141 27


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