Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the effect of a protein meal on secretin (IRS) concentration in dogs and humans using a radioimmunoassay of improved sensitivity (8 pg/ml). After a meal, pancreatic bicarbonate secretion (PBS) increased markedly and proximal duodenal pH decreased from 6.2 to 4.3. Portal and peripheral IRS concentrations, however, remained unchanged in eight dogs and five patients with cirrhosis of the liver. Similarly, an alkaline solution of sodium oleate (pH 9.2) stimulated PBS but not IRS. Intraduodenal administration of various amounts of HCl in dogs demonstrated that acid-stimulated PBS was invariably accompanied by rises in peripheral venous IRS concentration. We conclude that the postprandial stimulation of PBS involves mechanisms more complex than acid-stimulated secretin release.
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PMID:Effects of a protein meal, intraduodenal HCl, and oleic acid on portal and peripheral venous secretin and on pancreatic bicarbonate secretion. 2 27

Abnormally large duodenal aspirates have been reported in a large percentage of patients with cirrhosis of the liver. The source of this fluid has been variously ascribed to the liver and/or pancreas. The present study was undertaken to clarify its source. Eleven patients with cirrhosis of the liver and one with cholestatic hepatitis underwent an intraductal secretin test during endoscopic cannulation of the pancreatic duct. Six patients with cirrhosis had pancreatic hypersecretion ranging from 7.8 to 26.0 ml/min, while three patients demonstrated low secretory flow rates. Bile flow was negligible or nonexistent in ten patients, while in two others, larger but unmeasurable amounts of bile secretion were present. This study conclusively demonstrates that pancreatic hypersecretion may occur in patients with cirrhosis during secretin stimulation. Impaired metabolism of secretin or the associated pancreatic hypersecretion of early pancreatitis may be responsible for this finding.
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PMID:Pancreatic hypersecretion in liver disease. 61 31

A normal exocrine pancreatic function was demonstrated by the secretin-pancreozymin-test in five patients with Wilson's disease either without (n = 2) or with cirrhosis of the liver but without portal hypertension (n = 3). In another patient with cirrhosis of the liver without portal hypertension the pancreas was normal at post mortem examination. In two patients with cirrhosis of the liver and portal hypertension bicarbonate (n = 1) and amylase secretion (n = 2) were diminished. The regression of portal hypertension under therapy with penicillamine in one of the latter cases was paralleled by the return to normal of exocrine pancreatic function. It is concluded that exocrine pancreatic insufficiency in Wilson's disease is dependent on the development and the progression of chirrhosis of the liver and not due to a primary manifestation of the disease itself.
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PMID:[Involvement of the exocrine pancreas in Wilson's disease? (author's transl)]. 71 25

Exocrine pancreatic function was assessed by the standard test meal method of Lundh in a control group, and 13 patients with nonalcoholic, postnecrotic cirrhosis of the liver. In six of these patients, splenorenal shunts were performed and exocrine pancreatic function was assessed before and three months after operation. In three of the six, the secretin-pancreozymin stimulation test was also performed. An increased volume but normal trypsin output was observed in the unoperated cirrhotic patients. An increase both in volume and in trypsin was found in the cirrhotic patients after shunting using the test meal stimulation. There was no appreciable difference, however, when tested with secretin and pancreozymin. Hypersecretion in cirrhotics, with or without shunts, is probably due to a by-pass of the hepatic degradation of normal pancreatic secretogogues produced by the intestine.
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PMID:Exocrine pancreatic function in hepatic cirrhosis. 93 24

Sequential standard (1.0 U./kg.) and augmented (4.0-5.0 U./kg.) secretin response to the pancreas has been briefly compared in normal subjects and in patients with combinations of alcoholism, cirrhosis and alcoholic pancreatitis. The results of sequential testing led to the conclusion that, for clinical purposes, the standard test is adequate for the diagnosis of well established pancreatic pathologies causing gross destruction of the parenchyma. The augmented test is of particular value when the response to 1 U./kg. produced equivocal results, inasmuch as augmented stimulation enhances the masked secretory deficiency. The administration of the augmented stimulus to alcoholic patients yielded data which suggest a new hypothesis of pathogenesis for alcoholic pancreatitis, e.g., the postsecretin response pattern of minimal pancreatic inflammatory pathology is hypersecretion. Alcohol is thought to induce fatty degeneration of the pancreatic cell initially. Continued injury leads to necrosis and fibrosis.
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PMID:Standard and augmented secretin testing in chronic pancreatic alcoholic disease. 118 15

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

To confirm the respective influence of chronic alcoholism and liver disease on exocrine pancreatic function in cholecystokinin secretin (CS), tests were performed on patients with chronic liver cirrhosis (LC) and non-cirrhotic (nLC) disease of alcoholic (A) and nonalcoholic (nA) etiology. Results were compared in four subgroups (ALC, N = 26; AnLC, N = 45; nALC, N = 18; and nAnLC, N = 43). Volume of duodenal juice and bicarbonate output (BO) were increased and maximal bicarbonate concentration was decreased in ALC, compared with those in normal controls. Comparison of LC and nLC indicated that the volume, BO, and amylase output (AO) were greater in LC than in nLC of alcoholic etiology, but not in those of nonalcoholic etiology. The initial disappearance rate (KICG) of indocyanine green (ICG) excretion correlated with a parameter of CS test in alcoholic liver disease (vs. volume: r = -0.51, p less than 0.01 vs BO: r = -0.40, p less than 0.01), but not in nonalcoholic liver disease. Concurrent chronic pancreatitis with pain and definite exocrine insufficiency was observed in only one ALC patient and in four AnLC patients, but in none of the nonalcoholics. In alcoholic liver disease, exocrine pancreatic secretion tends to increase with severity of liver damage, but concurrence of definite chronic pancreatitis is not correlated with the severity.
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PMID:Exocrine pancreatic function in chronic liver diseases. 170 82

Plasma levels of glucagon, secretin, norepinephrine, arginine-vasopressin, and prostaglandin biosynthesis in the gastric mucosa were determined in cirrhotic patients with gastric vascular ectasia associated with hypoacidity, in cirrhotics without this lesion, and in healthy controls. Plasma concentrations of glucagon, secretin, and norepinephrine were similar in cirrhotics with gastric vascular ectasia and cirrhotics without this lesion, these concentrations being significantly higher (p less than 0.05) than in healthy controls. However, there was no significant difference between plasma levels of arginine-vasopressin in patients with cirrhosis (with or without gastric vascular ectasia) and those in healthy controls. The biosynthesis of prostaglandin E2 in the antrum of the gastric mucosa was significantly higher in cirrhotics with gastric vascular ectasia than in cirrhotics without this lesion (p less than 0.05) and healthy controls (p less than 0.005). Prostaglandin E2 in the corpus was significantly higher (p less than 0.05) in cirrhotics with gastric vascular ectasia than in healthy controls. The biosynthesis of 6-keto PGF1 alpha (a stable metabolite of prostacyclin) and PGF2 alpha in the corpus and antrum of gastric mucosa was not significantly different in cirrhotics with gastric vascular ectasia, cirrhotics without this lesion and healthy controls. Since prostaglandin E2 has a vasodilator and acid-inhibitory effect, we speculate that high content of this prostanoid in the gastric mucosa may play a role in the pathogenesis of ectatic capillaries and acid inhibition present in some cirrhotic patients.
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PMID:Increased gastric PGE2 biosynthesis in cirrhotic patients with gastric vascular ectasia. 230 36

Bile flow may be considerably increased in human cirrhosis. The mechanism of this increase has not been established. Two mechanisms have been proposed: a) increased canalicular filtration because of sinusoidal hypertension, or b) secretion by proliferated bile ductules. To distinguish between these two possibilities, we examined the determinants of bile secretion in rats with secondary biliary cirrhosis after bile duct obstruction. Sham-operated animals served as controls. Four weeks after bile duct ligation, all animals had cirrhosis. Bile flow was significantly higher and bile salt secretion significantly lower in cirrhotic animals than in controls. Biliary bicarbonate concentration was significantly higher in cirrhotic animals than in controls. Bile-to-plasma concentration ratio of erythritol was significantly lower in cirrhotic animals than in controls, suggesting a dilution of erythritol by a secretion distal to bile canaliculi. Bile-to-plasma ratio of sucrose was not significantly different in cirrhotics and controls, suggesting that paracellular permeability was not modified. Secretin, at the dose of 3 clinical units/100 g, induced an increase of approximately 75 percent in bile flow, and 70 percent in biliary bicarbonate concentration in cirrhotics. In conclusion, bile flow was increased in biliary cirrhosis in rats. The dilution of erythritol, the increase in biliary bicarbonate concentration and the increased response to secretin strongly suggest that increased choleresis was due, at least in part, to secretion by bile ductules or ducts. These results confirm that secondary biliary cirrhosis is a good experimental model for the study of alterations of bile secretion in cirrhosis.
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PMID:[An increase of choleresis in secondary biliary cirrhosis in rats is caused by bile duct secretion]. 235 Dec 43

To investigate whether the hypercholeresis seen in cirrhotic humans and animals is due to ductular proliferation or altered inactivation of secretin, or both, we studied the response of bile flow and biliary erythritol clearance to synthetic porcine secretin in rats rendered cirrhotic by chronic exposure to phenobarbital/carbon tetrachloride (n = 11) and untreated control rats (n = 5). Bile duct mass was determined morphometrically. Furthermore, plasma disappearance of secretin was measured by radioimmunoassay. Basal bile flow did not differ between the two groups. Whereas secretin had no effect in the control group, it stimulated bile flow by 49% +/- 33% in the cirrhotic group (p less than 0.001). Erythritol bile-to-plasma ratio was lower and biliary bicarbonate concentration higher in the cirrhotic rats, suggesting some ductular contribution to bile flow even in the absence of secretin. Biliary bicarbonate concentration did not increase further during secretin administration, whereas bile salt concentration decreased from 27 +/- 6 to 18 +/- 4 mM. The elimination half-life of secretin was not affected by cirrhosis, averaging 5 +/- 2 min in both groups. Bile duct volume was increased in cirrhotics (2.9% +/- 1.4% vs. 0.2% +/- 0.1%; p less than 0.01) and showed an excellent correlation with the maximal secretin-induced increment of bile flow. Our results suggest that the proliferating ductules contribute to bile flow and that increased secretin responsiveness is not due to altered pharmacokinetics in cirrhotic rat liver.
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PMID:Effect of secretin on bile formation in rats with cirrhosis of the liver: structure-function relationship. 232 32


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