Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008370 (cholestasis)
 9,378 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 22 patients with chronic pancreatitis and 16 patients with pancreas neoplasms gamma-glutamyltranspeptidase (GGTP) and alanine arylamidase (AAP) in serum were measured and the isoenzymes were determined by gel electrophoresis on Agar. No specific isoenzyme pattern was found for chronic pancreatic diseases in a comparative investigation with a group of 19 patients suffering from hepatobiliary diseases. Two fractions of AAP and GGTP isoenzymes were found on agar gel electrophoresis: alpha-1 and alpha-2 (GGTP between alpha-2 and beta-globulin). The alpha-1 fraction of AAP and GGTP seems to be a specific liver isoenzyme. The slower fraction of both enzymes was also found in chronic pancreatic diseases and cholestatic diseases as in neoplasms of liver, pancreas and biliary tract. Practical importance of the findings is diminished by large variation coefficients of the results. A significantly low ratio of alpha-1 to alpha-2 fraction (or beta-globulin) on electrophoresis of the isoenzymes of AAP and GGTP was found in the group with neoplasm of pancreas (especially neoplasm of the pancreas head) as compared to the group with intrahepatic cholestasis. The possible causes and diagnostic importance of the findings are discussed.
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PMID:[Isoenzymes of alanine arylamidase (AAP, EC 3.4.11.2) and gamma-glutamyltranspeptidase (GGTP, EC 2.3.2.2) in chronic pancreatitis and pancreas neoplasm (author's transl)]. 23 68

A pattern of results is reported which was found to be common among patients who had intrahepatic cholestasis (IHC) which was rarely found in patients with other hepatic conditions. The pattern was recognized from over 1000 cases suspected of hepatobiliary disease. 29 were diagnosed with IHC, and excluding 4, 25 revealed the following etiological pattern: chlorpromazine (12 patients); pregnancy and oral contraceptive use (8); and other (5). As opposed to patients with acute and chronic hepatic disease, IHC sufferers had relatively normal values for immunoglobulins and antibody titers. A disproportionate elevation of serum bilirubin vis-a-vis serum enzymatic activities separated potential IHC cases into intra- and extrahepatic cholestasis. The following factorial evaluations were useful in distinguishing hepatic disease states: 1) when the sum of the activities of serum alkaline phosphatase, 5'-nucleotidase, aspartate and alanine amiotransferases, and isocitrate dehydrogenase was divided by the serum bilirubin concentration, there was good resolution of the distinction between patients with IHC and those with primary biliary cirrhosis, early and late viral hepatitis, cholelithiasis, and pancreatic and bile duct cancers. 2) Resolution was also achieved when the numerator included alkaline phosphatase, 5'-nucleotidase, and aspartate aminotransferase, but not when alkaline phosphatase alone, or alkaline phosphatase combined with 5'-nucleotidase, was used. The essential lesion in IHC is an excretory defect.
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PMID:Biochemical features of intrahepatic cholestasis. 45 73

Protein hydrolysate-containing parenteral solutions have been reported to be hepatotoxic. Ten infants who were treated with a 20 percent glucose solution containing either 2.5 percent or 3.25 percent protein hydrolysate are reviewed. Their gestational ages were 30 to 40 weeks and births weights 1000 to 35000 g. Serum glutamate-oxaloacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), leucine amino peptidase (LAP) and bilirubin were measured serially. Serum amino acids were measured and consistently demonstrated decreased levels of isoleucine and increased aspartic acid, glutamic acid, serine, proline, glycine, alanine, threonine and lysine. The amino acid imbalances were associated with transaminase elevations in eight infants. Serum bilirubin levels increased in six patients and LAP in four. Liver biopsies from three patients showed minimal to moderate hepatic parenchymal disease with cholestasis.
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PMID:The hepatotoxicity of parenteral protein hydrolysate-containing solutions. 82 62

Hepatitis A is an acute, necroinflammatory disease of the liver which results from infection by the hepatitis A virus (HAV). The mean incubation period is approximately 30 days. Although the disease is usually self-limited, the severity of illness is age-dependent. In children, hepatitis A is usually asymptomatic, while in adults, symptomatic infection is characteristic and jaundice is common. Fulminant hepatitis A is rare and is also age-dependent. The onset of hepatitis A is often abrupt and characteristic prodromal symptoms are followed, within a few days to a week, by dark urine and jaundice. Mild to moderate tenderness over an enlarged liver is usually detected. Serum alanine and aspartate aminotransferase levels usually both rise rapidly during the prodromal period, reach peak levels and then decrease by approximately 75% per week. Serum bilirubin concentrations reach peak levels later and decline less rapidly than serum aminotransferases. Nonetheless, the period of jaundice persists for < 2 weeks in approximately 85% of cases. Nearly all adult patients with clinically apparent disease experience complete clinical recovery with restoration of normal serum bilirubin and aminotransferase values by 6 months. Relapses and prolonged cholestasis are unusual manifestations of hepatitis A, and even in these circumstances, recovery is the rule and chronic hepatitis is not seen. The diagnosis of hepatitis A requires the detection of immunoglobulin M antibody to HAV in a patient who presents with, or has recently had, clinical features of hepatitis (icteric or anicteric disease) or in an individual with inapparent, asymptomatic infection in whom serum aminotransferase elevations may be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical manifestations and diagnosis of hepatitis A virus infection. 133 49

Serum CA 19-9 and alpha-fetoprotein (AFP) levels were determined in 211 patients with liver cirrhosis and 27 with primary hepatocellular carcinoma (HCC) associated with liver cirrhosis. This was done to determine the usefulness of CA 19-9 level with respect to AFP level in distinguishing between these two illnesses, and to assess the influence of some clinical and biochemical variables on these tests in patients with liver cirrhosis with or without primary HCC. Pathologic AFP values were found in 23 of 27 (sensitivity, 85%) patients with HCC; CA 19-9 levels increased in only 12 of 27 (sensitivity, 44%) HCC patients, the values being comparable with those of patients with liver cirrhosis. In liver cirrhosis a substantial number of false-positive values was found for both markers, although they were higher for CA 19-9 (50 of 211 versus 39 of 211). In liver cirrhosis correlations were found between AFP level and alanine amino-transferase level; and between CA 19-9 level and (1) total bilirubin value, (2) alkaline phosphatase level, and (3) pseudocholinesterase level. The authors conclude that CA 19-9 level is a poor biochemical marker, inferior to AFP level, in the detection of a carcinomatous transformation of liver cirrhosis. The finding of false-positive AFP values in liver cirrhosis seems mainly attributable to cellular proliferation and necrosis. Cholestasis seems to greatly affect serum CA 19-9 level variations, probably by reducing its liver metabolism.
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PMID:Serum CA 19-9 and alpha-fetoprotein levels in primary hepatocellular carcinoma and liver cirrhosis. 138 Dec 71

Inflammation of the rat bile duct induced by administration of turpentine into it has been used to study the influence of the impaired duct on liver function. Turpentine was dissolved in olive oil 1:1000 and 1:500. A 2 h ligation of the bile duct was used to promote a local effect. Contemporary groups of intact, sham-operated, control rats (given 0.9% NaCl by intrabiliary injection) and animals with total chronic obstruction were compared to assess the significance of changes. Serum concentrations of total and conjugated bilirubin, cholesterol and creatinine, activities of S-alanine-aminotransferase, S-aspartate aminotransferase and alkaline phosphatase, mortality of rats, and also total body weight compared with the weight of the liver, were investigated on days 1, 4, 8, 12, 16, 32 and 64 after surgery and turpentine, or following ligation of the bile duct. An increase in bilirubin and cholesterol, an augmentation of enzymatic activity and the histological changes were indicative of hepatotoxicity or cholestasis. The turpentine concentration--effect, manifested in body-weight change, suggests some specificity of the effect. There were no changes in serum creatinine arterial blood pressure, heart rate or portal blood pressure, when turpentine was administered by the intrabiliary route. These results suggest primary liver damage.
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PMID:Liver damage induced by intrabiliary turpentine in rats. 197 95

Forty-four male and female subjects aged 22-57 years were studied. Thirteen patients had acute viral hepatitis, and eleven patients had cholestatic jaundice due to carcinoma of the head of the pancreas. Twenty healthy volunteers who served as controls were also included. In hepatitis patients, the mean plasma levels of total cholesterol (TC) and the high density lipoprotein (HDL)-phospholipid/phospholipid (HDLPL/PL) ratio were reduced, and HDL-cholesterol (HDLC), HDL-phospholipid (HDLPL) and the phospholipid/total cholesterol (PL/TC) ratio were normal, while total phospholipid (PL) levels and the HDLC/TC ratio were significantly increased compared to the control values. In patients with cholestatic jaundice the mean plasma total cholesterol, phospholipid and HDLC levels were elevated, and HDLPL/PL, HDLPL, HDLC/TC and PL/TC remained normal compared to the control values. A comparison within the patient groups showed that plasma TC, PL and HDLC levels were significantly increased in cholestatic jaundice when compared with the corresponding levels in hepatitis patients. The mean plasma levels of HDLPL, HDLC/TC and PL/TC did not show any significant variation within the patient groups. Alkaline phosphatase (ALP) correlated positively with TC, and total protein correlated negatively with TC and HDLPL, while albumin correlated negatively with TC, HDLC and HDLPL in cholestatic jaundice. Alanine amino-transferase (ALAT) also correlated positively with PL in cholestatic jaundice, while albumin correlated positively with TC in hepatitis. The results suggest that lipoproteins might be metabolized differently in these two forms of cholestasis.
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PMID:Changes in plasma high density lipoprotein cholesterol and phospholipid in acute viral hepatitis and cholestatic jaundice. 199 58

Serum concentrations of bile acids and bilirubin, and activity of alanine transferase and alkaline phosphatase as well as bile acid and bilirubin levels in duodenal contents were determined in 90 infants aged 1-44 weeks (including 49 under 10 weeks of age) admitted to hospital for prolonged jaundice. Infants with extrahepatic cholestasis were found to have statistically higher serum bile acid and bilirubin concentrations. Oral administration of cholestyramine produced a statistically significant decrease in serum bile acids and bilirubin in infants with intrahepatic cholestasis under 10 weeks of age. In 24 out of the 30 infants with biliary tract obstruction total absence of bile acids in the duodenal contents was demonstrated while in the others the concentration did not exceed 0.2 mmol/l. The mean bile acid concentration in infants with intrahepatic cholestasis was 2.81 mmol/l while in 8 infants out of the 60 bile acids were either absent or present in trace amounts. The method had an 84.4% sensitivity.
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PMID:Value of bile acid determination for the diagnosis of neonatal jaundice. 210 73

In selectively isolated basolateral (bILPM) and canalicular (cLPM) rat liver plasma membrane vesicles, the in vitro effect of cyclosporine A (CsA) on specific hepatic membrane transport processes was examined. CsA (0.1-200 microM) caused a concentration-dependent inhibition of initial rates of Na(+)-dependent taurocholate uptake in bILPM and cLPM vesicles and Na(+)-independent taurocholate efflux from cLPM vesicles. In contrast, CsA had no effect on Na(+)-dependent L-alanine uptake in bILPM and in cLPM vesicles. In addition, electroneutral pH gradient-driven Na+ uptake in bILPM vesicles was unaffected by CsA treatment. CsA-induced inhibition of taurocholate transport in bILPM and cLPM vesicles was competitive in nature. A hydroxylated (OL-17) and a N-demethylated (OL-21) metabolite of CsA had no effect on taurocholate transport in either membrane vesicle population. These findings suggest that the mechanism of CsA-induced cholestasis is, in part, the result of selective inhibition of bile acid transport by the parent compound at both domains of the hepatocyte plasma membrane.
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PMID:Inhibition of bile acid transport by cyclosporine A in rat liver plasma membrane vesicles. 235 33

Inhibition of Na+-K+-ATPase and sodium-dependent bile acid transport has been suggested as a mechanism for the cholestasis produced by certain drugs such as chlorpromazine. We examined the effects of chlorpromazine (and in selected studies, two of its metabolites) on Na+-K+-ATPase cation pumping (ouabain-suppressible 86Rb uptake), exchangeable intracellular sodium content, membrane potential (assessed by 36Cl- distribution), and sodium-dependent transport of taurocholate and alanine in primary cultures of rat hepatocytes. Chlorpromazine (10-300 microM), 7,8-dihydroxychlorpromazine (10-300 microM), and ouabain (0.1-2 mM), but not chlorpromazine sulfoxide, produced a concentration-dependent decrease in Na+-K+-ATPase cation pumping and an increase in intracellular sodium content. Chlorpromazine (100 microM) and ouabain (0.75 mM) also modestly decreased hepatocyte membrane potential. In further studies, chlorpromazine (75 and 100 microM) and ouabain (0.1, 0.5, and 0.75 mM) decreased initial sodium-dependent uptake rates of taurocholate and alanine by 18-63%. Although the steady-state intracellular content of alanine was decreased 25-53% by both agents, chlorpromazine increased the steady-state content of taurocholate by 171% and decreased taurocholate efflux, apparently related to partitioning of taurocholate into a large, slowly turning over intracellular pool. These studies provide direct evidence that chlorpromazine inhibits Na+-K+-ATPase cation pumping in intact cells and that partial inhibition of Na+-K+-ATPase cation pumping is associated with a reduction of both the electrochemical sodium gradient and sodium-dependent solute transport. These effects of chlorpromazine may contribute to chlorpromazine-induced cholestasis in animals and humans.
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PMID:Effects of chlorpromazine on Na+-K+-ATPase pumping and solute transport in rat hepatocytes. 244 5


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