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 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

Basal plasma cholecystokinin levels were measured by a bioassay using dispersed rat pancreatic acini in various digestive diseases and compared with corresponding values by CCK-8 specific radioimmunoassay. The mean basal level in healthy volunteers was 0.40 +/- 0.06 pM. The basal level in liver cirrhosis was significantly elevated to 0.92 +/- 0.14 pM. The patients with cholestasis, that is, primary biliary cirrhosis and obstructive jaundice due to choledocholithiasis, bile duct cancer or lymph node metastasis , had markedly increased basal plasma CCK-8 like bioactivities from 1.88 pM to more than 25 pM. These CCK bioactivities were not correlative with CCK immunoreactivities. It was concluded not only that basal plasma CCK in patients with bile flow disturbance were truly increased, but also that interfering substances of the bioassay might appear in the plasma of these patients.
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PMID:[Basal plasma cholecystokinin levels in digestive diseases--comparison between CCK-8 like bioactivity by bioassay and CCK immunoreactivity by radioimmunoassay]. 260 Nov 19

Pancreatic endocrine function in liver cirrhosis was examined in rats both in vivo and in vitro. Experimental liver cirrhosis was induced by subcutaneous injections of 50% carbon tetrachloride in a dose of 2 mL/kg body weight twice a week for 16 weeks. Control rats received a similar dose of olive oil during the same period. In cirrhotic rats, immunoreactive insulin contents in the pancreas were significantly lower, whereas immunoreactive glucagon contents were about threefold higher than those of control rats. In the first part of this study, insulin and glucagon concentrations in both jugular and portal venous blood at basal conditions and after oral glucose loading were simultaneously determined in vivo. Peripheral insulin levels, both before and after glucose loading, were higher, whereas portal insulin concentrations were lower in cirrhotic rats than in the control rats. In contrast, glucagon levels in both the peripheral and portal veins were significantly higher in cirrhotic rats than in control rats. In the second part, isolated perfused pancreata were prepared from cirrhotic and control rats to further characterize the endocrine function of cirrhotic rat pancreas. Insulin secretion in response to 16.7 mmol/L glucose and 100 pmol/L cholecystokinin-octapeptide both were 40% lower in cirrhotic rats than in controls. In contrast, there was no significant difference in arginine-stimulated insulin release between the two groups. However, glucagon secretion in response to 20 mmol/L arginine was 40% higher in cirrhotic rats. If sensitivity is defined as the hormone release proportional to the pancreatic contents, then A and B cells in the cirrhotic rats had normal sensitivity to both glucose and cholecystokinin-octapeptide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pancreatic endocrine function in cirrhotic rats. 304 24

For exploration on the elimination of cholecystokinin from the circulation, the disappearance half-time of cholecystokinin-octapeptide was estimated with cholecystokinin specific radioimmunoassay in normal subjects and patients with chronic renal failure and with hepatic cirrhosis. With a brief infusion of 30.4 ng/kg of cholecystokinin-octapeptide for 2 min, plasma cholecystokinin level rose from 16.1 +/- 3.6 pg/ml (mean +/- SE) to 216.5 +/- 6.1 pg/ml at 3 min after starting infusion, and decreased rapidly in a single exponential fashion for 10 min in hepatic cirrhosis. The disappearance half-time of cholecystokinin-octapeptide in patients with hepatic cirrhosis was 2.45 +/- 0.07 min, and it was significantly longer than that in normal subjects (1.30 +/- 0.07) or patients with chronic renal failure (1.70 +/- 0.11). These findings suggest that the liver plays a major role in cholecystokinin-octapeptide elimination in humans.
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PMID:Marked prolongation in disappearance half-time of plasma cholecystokinin-octapeptide in patients with hepatic cirrhosis. 401 6

Secretion of bile salts into the duodenum was studied in eight normal subjects, in 10 patients with cirrhosis, and in two cholecystectomized subjects. Duodenal juice was aspirated continuously through a double-lumen tube during an unstimulated period, after an intravenous injection of pancreozymin/cholecystokinin, and during a continuous intravenous infusion of secretin given at a rate of 3 units per kilogram body weight per hour. Precautions were taken to try to ensure quantitative recovery during the studies, and recovery of an infused nonabsorbable marker was greater than 80% in all subjects. Secretin induced a flow of a greater volume of juice in the cirrhotic patients than in the normal group (49 to 57 ml per 10 minutes compared with 28 to 49 ml per 10 minutes). This change may have resulted from a higher effective dose of secretin if it is assumed that the cirrhotic liver fails to catabolize secretin. The bile acid response to pancreozymin/cholecystokinin followed by secretin in the cirrhotic subjects resembled that seen in patients after cholecystectomy in whom pancreozymin/cholecystokinin induces only a slight increase in bile salt output but in whom the output of bile salts during rest and secretin stimulation is markedly greater than normal. This response in cirrhosis is probably best interpreted as due to impaired function of the gallbladder. The total amount of bile salt liberated over the two hours of the test in the cirrhotic patients was similar to normal The concentration of bile salt after pancreozymin/cholecystokinin was less than in normal subjects, but similar to that in cholecystectomized patients. It is unlikely therefore that deficient output or concentration of bile salt can be held responsible for steatorrhea in cirrhosis. THERE WAS A MARKED DECREASE IN THE DEOXYCHOLATE CONJUGATES AND A REDUCTION IN THE GLYCINE: taurine ratio in the bile of cirrhotic patients. The former change may reflect a change in bacterial flora and the latter a defect in hepatic conjugating mechanisms.
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PMID:Bile salt secretion in cirrhosis of the liver. 544 81

A highly sensitive and precise radioimmunoassay system for plasma cholecystokinin (CCK) was developed with the anti-CCK-8 specific antiserum which raised against N-terminal amino acids residue of sulfated CCK-8 and reacted with CCK-8, CCK-33, and CCK-39 but not with gastrin and its related peptides. Mean concentration of the fasting plasma CCK determined with this method using CCK-8 as standard was 12.9 +/- 5.9 pg/ml in normal subjects (n = 26), and in patients with hepatic cirrhosis it was significantly higher (36.7 +/- 16.9 pg/ml, n = 9, p less than 0.01) than in normal subjects. In six young healthy volunteers, intraduodenal infusion of fat caused a significant increase (p less than 0.05) of plasma CCK from a basal level of 8.0 pg/ml to a peak of 43.0 +/- 12.0 pg/ml at 20 min after starting of infusion. In the same subjects, a significant increase of plasma CCK was also observed by amino acids infusion, but no elevation of plasma CCK level was found during intraduodenal acidification.
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PMID:Plasma cholecystokinin responses after ingestion of liquid meal and intraduodenal infusion of fat, amino acids, or hydrochloric acid in man: analysis with region specific radioimmunoassay. 663 57

In 12 patients with Laennec's cirrhosis conjugated cholic acid was measured by radioimmunoassay simultaneously in the portal vein, the aorta, and the hepatic vein. Furthermore, the concentration was measured for 90 minutes after i. v. injection of cholecystokinin. In the fasting patient the porto-venous extraction ratio was 0.45 (SD 0.23) and the arterio-venous extraction ratio was 0.24 (SD 0,21). 15-30 minutes after cholecystokinin the bile acid concentration significantly increased. In this time the porto-venous extraction ratio rose to 0.71 while the aorto-venous extraction ratio was different. These results agree with the hemodynamics found in cirrhosis. After cholecystokinin the increase in the extraction ratio account for the blood loss by porto venous shunts which corresponds to an increase of the portal compartment.
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PMID:[Conjugated cholic acid in the portal vein, aorta and hepatic vein in patients with alcohol toxic liver cirrhosis]. 664 39

We have studied the volume, protein concentration, total protein, and chymotrypsin and trypsin outputs in pure pancreatic juice (PPJ) following endoscopic cannulation of the pancreatic duct in 11 male and 2 female patients with advanced alcoholic cirrhosis (AC). Results were compared to those obtained from 21 nonalcoholic volunteers (NAV) and 26 chronic alcoholic (CA) patients without cirrhosis. Intravenous stimulation with secretin followed 10 min later by intravenous cholecystokinin-pancreozymin (CCK-PZ) resulted in highly significant increases in volumes during both phases of pancreatic stimulation in AC compared to NAV and CA. Protein concentration and total output during secretin stimulation was not different among the three groups. During CCK-PZ stimulation, CA exhibited a significant elevation in protein concentration and total output compared to NAV and AC. Although total chymotrypsin output was lower in secretin-stimulated CA than other groups, no other differences between the groups were observed in either of the hormone-stimulation phases. Marked elevations in trypsin output were observed in secretin-stimulated AC and in CCK-PZ-stimulated AC and CA. The high PPJ volume and the relatively low protein concentration observed in AC may effect a washout phenomenon resulting in a decreased tendency for ductal protein precipitation in these patients.
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PMID:Pancreatic secretion after secretin and cholecystokinin stimulation in chronic alcoholics with and without cirrhosis. 665 99

Defective gallbladder emptying has been proposed as a possible accessory pathogenetic factor to explain the increased prevalence of gallstones in liver cirrhosis. In this study we have evaluated the fasting volume and the meal-stimulated emptying of the gallbladder, the plasma levels of estradiol and progesterone, and the basal and postprandial secretion of cholecystokinin in Child A cirrhotic patients compared to normal subjects. Basal (42.2 +/- 27 vs 22.8 +/- 8.4 ml) (P < 0.002) and residual (8.4 +/- 8.7 vs 4.6 +/- 3.8 ml) (P < 0.05) gallbladder volumes were higher in cirrhotics but neither the integrated gallbladder response to meal nor the maximal percentage of emptying was significantly different. Circulating estradiol and progesterone was slightly increased in only 1/13 and 5/13 cirrhotics, respectively. In eight cirrhotics and seven normals taken from the overall populations, the secretion of cholecystokinin was also measured. The fasting plasma level of cholecystokinin was higher in the cirrhotics (6.71 +/- 5.08 vs 2.02 +/- 0.46 pmol/liter) (P < 0.01). The meal-stimulated integrated plasma cholecystokinin response also was greater in cirrhotics (438.5 +/- 615 pmol/liter/270 min) than in normals (153 +/- 170.4 pmol/liter/270 min), but this difference was not significant because of the small study population. In spite of a normal kinetics of postprandial emptying, cirrhotic patients show increased fasting gallbladder volume and increased plasma levels of basal and postprandial cholecystokinin. Circulating estradiol and progesterone do not seem to be responsible for the large gallbladder volume found in liver cirrhosis.
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PMID:Gallbladder emptying, plasma levels of estradiol and progesterone, and cholecystokinin secretion in liver cirrhosis. 785 Dec 11


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