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

Complex evaluation of secretin-pancreozymin test data with multivariate statistical methods was performed in patients with pancreatic insufficiency and in controls. The centroid, the nearest neighbour methods and the linear discriminant analysis led to the correct diagnosis in 84, 77 and 92%, respectively, when the overall responses to synthetic secretin plus cholecystokinin-octapeptide were evaluated. Results of individual stimulations were less precise. The linear discriminant analysis also successfully separated the patients with mild chronic pancreatitis from the healthy subjects, and seems to provide a useful support in medical diagnosis, particularly in controversial cases.
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PMID:Complex evaluation of secretin-pancreozymin test data by multivariate statistical pattern recognition methods. 368 Oct 25

Chronic pancreatitis has been reported to be associated with an increased secretion of calcium in pancreatic juice. To determine whether estimation of duodenal calcium may be useful for diagnosing chronic pancreatitis, we compared duodenal calcium output in patients with chronic pancreatitis and in subjects without pancreatic disease, during intravenous infusion of secretion alone, with calcium, or with cholecystokinin-pancreozymin (CCK-PZ). Duodenal calcium output increased during infusion of both calcium and CCK-PZ to a similar extent in chronic pancreatitis and controls. Overall, duodenal output of chymotrypsin was markedly lower in chronic pancreatitis; however, chymotrypsin output increased in response to both intravenous calcium and CCK-PZ in both groups. Bilirubin output increased in both groups during calcium infusion, but this increase was significantly reduced in chronic pancreatitis; in contrast, CCK-PZ caused a similar increase in both groups. The high calcium output observed in hypercalcemia in the presence of low enzyme output suggests increased pancreatic secretion of enzyme-independent calcium in chronic pancreatitis. However, the difference is obscured by biliary calcium, which is secreted in much higher concentrations. Thus, duodenal calcium determination does not appear to be a useful diagnostic test in chronic pancreatitis.
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PMID:Duodenal calcium in chronic pancreatitis: is it of diagnostic value? 370 99

Thirty-three patients with chronic pancreatitis were studied in an effort to correlate release of gastrointestinal hormones (GIH) with the degree of pancreatic insufficiency. A prospective examination was conducted of fat-stimulated release of pancreatic polypeptide (PP), cholecystokinin (CCK), and neurotensin. Seventy-two-hour fecal fat determination, endoscopic retrograde pancreatography (ERP), and the bentiromide-PABA test were used to correlate the clinical stage of disease. The ERP was classified as positive only if the changes were advanced (or "marked") according to the Cambridge Classification. Five patients were defined to have mild disease, 13 moderate, and 15 severe. Any patient with clinical evidence of chronic pancreatitis and ERP changes that were less than advanced and had normal fecal fat and bentiromide tests received a grade of mild. Patients with one abnormal test were graded moderate, and those with two or three abnormal results were graded severe. In the 33 patients, the integrated 60-minute release of pancreatic polypeptide (PP) was 37.4 +/- 6.1 ng-60 min/ml in those five patients with mild disease, 102.3 +/- 10.3 ng-60 min/ml in the 13 patients with moderate disease, and 7.6 +/- 2.2 ng-60 min/ml in the 15 patients with severe disease. The integrated 60-minute release of neurotensin was 3.8 +/- 0.4 ng-60 min/ml in mild disease, 2.0 +/- 0.3 ng-60 min/ml in moderate disease, and 0.2 +/- 0.1 ng-60 min/ml in severe disease. CCK release did not correlate with the severity of disease. Enhanced release of PP appeared to correlate well with moderate stage of chronic pancreatitis, and depressed PP release with severe disease. Stimulated levels of PP and neurotensin appear to be useful in the diagnosis and staging of chronic pancreatitis. It is concluded that measurement of fat-stimulated release of PP and neurotensin may be useful to assess severity of disease in patients with chronic pancreatitis.
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PMID:Diagnostic role of gastrointestinal hormones in patients with chronic pancreatitis. 376 78

Using validated double-marker techniques to quantitate tryptic secretion we found that the mean 10-min output of trypsin in duodenal juice after a test meal was very similar to the peak 10-min output of trypsin after pancreozymin (2 Crick-Harper-Raper units/kg, Boots) both in controls as well as in non-diabetic patients with idiopathic chronic pancreatitis. These results show that the disproportionate reduction in mean tryptic activity after endogenous compared with exogenous stimulation in chronic pancreatitis is not due to impaired release of cholecystokinin-pancreozymin from the small intestine, nor to refractoriness of the pancreas to endogenously released hormone: instead, it is due to overdilution of secreted pancreatic enzymes because of accelerated gastric emptying, with or without gastric acid hypersecretion.
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PMID:Quantitation of tryptic responses to endogenous and exogenous stimulation in chronic pancreatitis. 377 Mar 23

Discriminant analysis was used to interpret the results of the secretin-cholecystokinin (CCK) test in the diagnosis of chronic pancreatitis. An allocation rule based on the use of two test variables--mean chymotrypsin concentration and peak bicarbonate output--was constructed to distinguish between 63 patients with chronic pancreatitis and 68 patients without organic disease. These latter patients had signs and symptoms similar to those of the patients with chronic pancreatitis and were used as controls. The allocation rule was applied to a larger set of individuals, including 105 patients with various other diseases. The sensitivity of the test was 83%, and the specificity was 89%. With a prevalence of chronic pancreatitis of 27% in this set of individuals, the positive predictive value was 73%, the negative predictive value was 93%, and the accuracy rate 87%. This diagnostic performance of the secretin-CCK test gives the test a meaningful place in the examination of patients suspected of having chronic pancreatitis.
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PMID:Evaluation of the secretin-cholecystokinin test for chronic pancreatitis by discriminant analysis. 395 50

Previous studies have suggested that intraduodenal protease suppression of pancreatic exocrine secretion may be mediated through cholecystokinin (CCK) release. Our study compares basal plasma immunoreactive CCK concentrations in normal human subjects with those obtained in patients with chronic pancreatitis. Fasting plasma samples were collected from 18 normal subjects and from 18 patients with chronic pancreatitis. Eight patients had mild to moderate pancreatic exocrine impairment, and 10 had severe exocrine insufficiency. Venous plasma immunoreactive CCK concentrations were measured with two distinct peptide region-specific antibodies. Basal plasma CCK concentration in controls was 14.3 +/- 1.3 fmol/ml (mean +/- SEM), a value significantly less than that obtained in all patients with chronic pancreatitis, 30.1 +/- 4.0 fmol/ml (p less than 0.001). Patients with mild to moderate impairment had a fasting plasma CCK concentration of 32.8 +/- 7.9 fmol/ml (vs. control p less than 0.01), and those with severe disease 27.9 +/- 3.6 fmol/ml (vs. control p less than 0.001). In five patients with mild to moderate impairment of exocrine function and pancreatic extract-responsive abdominal pain, there was a 39 +/- 11% decrease in basal CCK levels during extract therapy (p less than 0.05). Results of this study indicate that pancreatic exocrine impairment is associated with elevated basal CCK levels, which may reflect a failure to provide feedback downmodulation of CCK release.
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PMID:Elevated fasting cholecystokinin levels in pancreatic exocrine impairment: evidence to support feedback regulation. 397 64

In a prospective evaluation of patients suspected of having chronic pancreatitis, synthesis of pancreatic enzymes was measured by means of the incorporation of selenium-75-labelled methionine into the proteins of duodenal aspirate during stimulation of pancreatic secretion with secretin (1 CU X kg-1 X h-1) plus cholecystokinin (CCK) (1 IDU X kg-1 X h-1). The rate of pancreatic enzyme synthesis was increased in patients with chronic pancreatitis. Measurement of pancreatic enzyme synthesis was more sensitive in the detection of chronic pancreatitis than either the bicarbonate or the trypsin secretory response to secretin plus CCK. A combination of the bicarbonate secretory response with measurement of the rate of enzyme synthesis provided a positive predictive power of 100% when both tests were abnormal and a negative predictive power of 100% when both tests were normal, so that the combined test can be recommended both for excluding and confirming the presence of chronic pancreatitis.
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PMID:Pancreatic enzyme synthesis in pancreatic disease. 403 92

Using a sensitive and specific radioimmunoassay for cholecystokinin (CCK) we have measured plasma CCK levels in patients with and without chronic pancreatitis. All patients suffered from steatorrhea. The basal plasma values in patients with chronic pancreatitis (n = 10) were significantly higher compared with a control group of 40 normal subjects. After ingestion of a test meal peak plasma levels of CCK were significantly higher than in controls, but the integrated CCK release did not differ from the normal subjects. The findings indicate a close relationship between plasma CCK concentration and exocrine pancreatic function.
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PMID:Plasma cholecystokinin levels in patients with chronic pancreatitis. 404 64

Postprandial responses of plasma cholecystokinin (CCK) in patients with severe chronic pancreatitis (n = 7) were studied. Plasma CCK level rose from 11.2 +/- 1.8 pg/ml at the basal level to a maximum of 23.3 +/- 3.0 pg/ml at 10 min after the ingestion of a liquid meal in healthy subjects (n = 6). However, such significant plasma CCK response to the meal was not observed in patients with chronic pancreatitis in whom CCK levels rose from a basal level of 9.7 +/- 0.91 pg/ml to a peak of 13.8 +/- 1.6 pg/ml at 60 min. It is suggested that the low response of CCK after the meal might reflect impaired function of the enteropancreatic axis to intraluminal stimuli in patients with severe chronic pancreatitis.
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PMID:Low plasma cholecystokinin response after ingestion of a test meal in patients with chronic pancreatitis. 407

Exocrine pancreatic function was evaluated by a Lundh meal test and a secretin-cholecystokinin test in 16 patients with chronic pancreatitis. B cell function was assessed by measuring the concentration of C-peptide after stimulation with oral glucose and intravenous glucagon. The Cc-peptide response to intravenous glucagon and oral glucose was closely correlated (r = 0.88, p less than 0.01). Plasma C-peptide after glucagon was significantly correlated to the post-prandial concentration of lipase (r = 0.72, p less than 0.001), amylase (r = 0.64, p less than 0.05) and to amylase output (r = 0.64, p less than 0.05). Eight out of nine patients treated with insulin had residual B cell function, but it diminished significantly with increasing duration of diabetes. We conclude that B cell function is correlated to pancreatic enzyme secretion and that patients with insulin-treated diabetes secondary to chronic pancreatitis have a residual insulin secretion similar to that of patients with Type 1 (insulin-dependent) diabetes.
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PMID:B cell function in patients with chronic pancreatitis and its relation to exocrine pancreatic function. 618 47


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