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)

Salicylamide glucuronide (SAMG) in 0-6 and 6-12 hours-urine specimens was determined after oral administration of salicylamide in 7 normal volunteers (NV), in 51 cases of various liver diseases and hyperbilirubinemias, and in 19 cases after drug administration, to predict the in vivo drug metabolism in man and its change by drugs. Maximal glucuronide formation was obtained by 1.0 g of salicylamide administered to NV; thus, this dosage was used in the present study. SAMG as percent of total salicylamide, the percent of SAMG, from 0-6 hours-urine specimens was high and constant in NV (71.3 +/- 8.3 (Mean +/- S.D.)). 0-0.08% of the total salicylamide was confirmed as free salicylamide in 0-12 hours-urine specimens of NV. The percent of SAMG of 0-6 hours-urine specimens was 57.2 +/- 8.6 in acute hepatitis, 66.6 +/- 10.9 in chronic hepatitis, and 48.6 +/- 10.7 in liver cirrhosis (mean +/- S.D.). Free salicylamide increased slightly in liver diseases. Serum bilirubin levels tended to be inversely correlated with the percent of SAMG. In most cases of Gilbert's syndrome, the percent of SAMG remained at a normal level. The percent of SAMG in cases with unconjugated hyperbilirubinemias of other geneses were almost within normal limits. Bucolome and phenobarbital increased the percent of SAMG in patients with various liver diseases. After rifampicin or phenytoin administration, the percent of SAMG of the patients with lung tuberculosis or epilepsy did not surpass that of NV.
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PMID:Salycylamide glucuronide formation in liver disease and its change by drugs. 1 Feb 19

Serum gamma-glutamyl transpeptidase (gamma-GT) level was estimated in 132 patients with different liver diseases (chronic persistent and chronic active hepatitis, postnecrotic cirrhosis, chronic alcholic hepatitis and alcoholic cirrhosis, cholestasis syndrome, fatty liver, Gilbert disease) and malignancies with and without liver involvement. The gamma-GT levels were compared with the values for serum bilirubin, transaminases (GOT, GPT) and alkaline phosphatase in the same patients. gamma-GT values were normal in chronic persistent hepatitis and increased in chronic active hepatitis. Very high activities were measured in chronic alcoholic cirrhosis in contrast to postnecrotic cirrhosis. gamma-GT proved to be more sensitive than alkaline phosphate as an index of cholestasis and liver involvement in malignancies. It is suggested that gamma-GT activity offers valuable aid in differential diagnostics of liver-diseases. gamma-GT being an inducible enzyme, its activity may be raised by enzyme inducing drugs also in subjects without liver disease.
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PMID:Serum gamma-glutamyl transpeptidase: its clinical significance. 2 44

The mechanism by which intravenous administration of nicotinic acid (NA) increases serum unconjugated bilirubin in patients with the Gilbert's syndrome has been investigated. Studies using the technique of percutaneous transhepatic catheterization of the splenic vein and coil planet centrifuge suggested that following intravenous injection of NA some of the circulating erythrocytes were rendered osmotically fragile and trapped by the spleen and that unconjugated bilirubin increased in the splenic vein blood. In patients with liver cirrhosis, the increments of unconjugated bilirubin were closely correlated with the weights of the spleens removed for the management of varices. In rats, intravenous NA injection enhanced heme oxygenase activities in the spleen, but not uridine-5'-diphosphate (UDP)-glucuronyltransferase activity in the liver. These results are consistent with the hypothesis that NA-induced unconjugated hyperbilirubinemia is a result of complex reactions which include increased erythrocyte fragility, increased splenic heme oxygenase activity, and increased formation of bilirubin in the spleen.
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PMID:Studies on nicotinic acid interaction with bilirubin metabolism. 48 25

Using a micromethod, hepatic bilirubin UDP-glucuronyl transferase has been assayed in percutaneous needle biopsy samples obtained from patients with infectious hepatitis, postnecrotic cirrhosis, Gilbert's disease, noncirrhotic portal fibrosis (NCPF), granuloma of the liver, and extrahepatic portal vein obstruction. The results were compared with those obtained from 10 control subjects. Patients with cirrhosis and infectious hepatitis revealed normal bilirubin transferase levels, whereas those with Gilbert's disease showed significantly low enzyme levels. Many patients with NCPF, some with extrahepatic portal vein obstruction, and patients with granulomatous involvement of the liver demonstrated significantly low levels. This low hepatitic-enzyme activity was not associated with hyperbilirubinemia. The mechanism of such low values in NCPF and other disorders is not known. It is postulated that low heaptic-enzyme activity in noncirrhotic portal fibrosis is due to sparse smooth endoplasmic reticulum. This study also emphasizes that serum bilirubin may remain normal with very low hepatic-enzyme activity. Although induction of the microsomal enzyme bilirubin transferase was observed following phenobarbitone administration in noncirrhotic portal fibrosis, this was not apparent in patients with cirrhosis, possibly due to maximal enzyme induction having been achieved by endogenous substrate.
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PMID:Estimation of hepatic bilirubin UDP-glucuronyl transferase in patients with noncirrhotic portal fibrosis and liver disease: Significance and limitations. 81 Nov 12

Increased liver copper concentration and raised serum ceruloplasmin were demonstrated in primary biliary cirrhosis and disorders of the biliary tract, and occasionally in chronic active hepatitis and cirrhosis of the liver. Eight of 13 patients with primary biliary cirrhosis had liver copper content as high as seen in patients with hepatolenticular degeneration (is greater than 250 mjg/g dry weight). Normal liver content was found in patients with acute hepatitis, steatosis of the liver, hepatic amuloidosis, haemochromatosis, and Gilbert's syndrome. The urinary copper excretion was increased (is greater than 75 mjg/24 h) in half the patients with primary biliary cirrhosis and occasionally in the other patient groups. Serum ceruloplasmin was raised in more than half of all patients, and none had levels below the reference range. Raised heaptic copper content did not always coincide with enhanced urinary copper excretion, but was significantly correlated with this parameter and also with ceruloplasmin, alkaline phosphatases, and vitamin-K-dependent clotting factors, but not with ALAT. Combination of laboratory data, as found in typical cases of hepatolenticular degeneration, was not observed in this study, including 66 patients.
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PMID:Hepatic copper content, urinary copper excretion, and serum ceruloplasmin in liver disease. 83 74

The diagnosis of viral hepatitis was not confirmed in 2976 (22.79%) out of the admitted to the hospital patients for a period of 15 years. What impresses is the percentage growth for the last several years, reaching to 30. This, on one hand is associated with the greater exigence of HEI and with the strong fear of that disease as well as with the improved diagnostic possibilities of the infectious diseases wards on the other. In fact, almost all patients with icterus were admitted to infectious diseases wards, where the differential diagnosis of icterus was made. The first place among the false diagnoses is occupied by liver-bile diseases, progressing with icterus-50.81%, (cholelithiasis-29%, carcinoma-11%, cirrhosis, chronic hepatitis, steatosis, cholangiohepatitis, pancreatitis, etc-10.8%). Second, according to incidence, come the gastrointestinal diseases-13.51%, grippe and grippe-like diseases-13.44%, lung diseases-5.21%, blood-3.80%, heart-3.16%, toxic hepatitis 3.26%, etc. Thirty cases of infectious mononucleosis with icterus are reported as well as 17 patients with liver etzymopathies, syndrome of Dublin--Johnson--6 and Gilbert--Meulengracht syndrome--11. Viral hepatitis diagnosis is not always easy and in many cases it requires a complex of laboratory and other investigations and many years of experience. However, the false diagnosis could be reduced with more than a half with the careful consideration of the epidemic situation, anamnestic and clinical data.
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PMID:[Diagnostic problems of viral hepatitis]. 89 23

A discussion is made of the basic peculiarties and differences in the clinico-laboratory profile in various forms of pre- and postmicrosome jaundice. The importance of direct to total bilirubin ratio, and of quantitative bilirubin and urobilinogen bodies' determination in the urine is stressed. Bile pigments conjugation by the hepatic cells and free bilirubin conversion to glucuronose may be also assayed by resorting to some additional tests. The test with N-acetyl-paraaminophenol (NAPA) provides for an indirect assessment of the liver's glucuronidase function and has a good informative value. It is optimally characterized by the percentage of free (non-conjugated) NAPA with respect to the total. The latter indicator is normal in chronic hepatitis and in Dubin-Johnson's syndrome, and is at the uppermost normal limit in hepatic cirrhosis and cholestatic jaundice. It is strongly increased (in the average three times with respect to normal values) in Gilbert's disease and posthepatitis hyperbilirubinemia (PHHB). It affords some information on the severity of the defect in transport of bile pigments in the mentioned affections. In hemolytic jaundice a normal percentage of free NAPA is usually found. Glucuronose conversion of bilirubin hardly plays an essential role in the pathogenesis of hyperbilirubinemia i the listed above diseases. This is also confirmed by the NAPA test, performed subsequent to novobiocin loading. The percentare of free NAPA under the conditions just outlined is furthermore increased in Gilbert's disease and PHHB, while in hemolytic jaundice it remains within normal limits. In Gibert's disease and PHHB, a strongly pronounced delay in the excretion of substances is noted. Not infrequently, a similar disorder is also observed in hepatic cirrhosis. It is interpreted as an expression of an overall disturbance in hepatic blood flow and function of the heavily affected hepatic parenchyma.
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PMID:[Study of liver glucuronidase function in indirect hyperbilirubinemia and liver cirrhosis]. 123 97

Sulfur amino acid metabolism was studied in patients with mild to severe forms of liver dysfunction and compared with that of healthy controls. Patients with mild liver dysfunction (for example, Gilbert's syndrome) had a normal sulfur amino acid metabolism. With increased inflammatory activity and cirrhosis (for example, chronic active hepatitis, alcohol-induced cirrhosis, and hepatic coma) a decreased ability to metabolize methionine (to cysteine, with cystathionine accumulation) and cysteine (to inorganic sulfate, with thiosulfate and N-acetylcysteine accumulation) was found. In contrast, transaminative metabolism of sulfur amino acids was preserved in patients with advanced forms of liver dysfunction, suggesting that transamination of sulfur amino acids is performed not only in the liver but also in extrahepatic tissues. Some implications of these findings are discussed.
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PMID:Sulfur amino acid metabolism in hepatobiliary disorders. 152 76

Black and brown pigment gallstones are morphologically, compositionally, and clinically distinct. Black stones form primarily in the gallbladder in sterile bile and are associated with advanced age, chronic hemolysis, alcoholism, cirrhosis, pancreatitis, and total parenteral nutrition. Brown stones form not only within the gallbladder but also within the intrahepatic and extrahepatic ducts; they are uniformly infected with enteric bacteria and are usually associated with ascending cholangitis. Brown stones are related to juxtapapillary duodenal diverticula and are the predominant type of de novo common bile duct stones. Cholecystectomy is usually curative in black pigment stone disease, whereas stones often recur after cholecystectomy for brown stone disease. The pathogenesis of black stones is probably related to nonbacterial, nonenzymatic hydrolysis of bilirubin conjugates. At the pH of bile, this results in two monohydrogenated bilirubin anions that precipitate with calcium ions. Bilirubin monoconjugates that are increased in several conditions, such as Gilbert's syndrome and chronic hemolysis, may play a pivotal role in black stone formation as a source of unconjugated monohydrogenated bilirubin and as a possible co-precipitant with calcium. The precipitation of calcium carbonate and phosphate is influenced by local gallbladder factors. Brown pigment stones are formed in bile infected with enteric bacteria that elaborate hydrolytic enzymes: beta-glucuronidase, phospholipase A, and conjugated bile acid hydrolase. The resulting anions of bilirubin and fatty acids form insoluble calcium salts. We used nb/nb mice with a chronic hemolytic anemia as a model of hemolysis-induced black stone disease. The presence of 40% bilirubin monoconjugates in mouse gallstones indicated the importance of this moiety in the pathogenesis of black stones. Other data obtained by marrow transplantation experiments in mice revealed the relative importance of genotype versus the hemolytic anemia on determinants such as biliary bile acid composition and mucin secretory glands in the mouse gallbladder neck. Additional physical chemical studies of the interaction of unconjugated bilirubin in model bile solutions will be helpful in further delineating the pathogenesis of both black and brown pigment gallstones.
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PMID:Pigment gallstone disease. 202 17

The determination of direct and indirect-reacting bilirubin fractions by diazo procedures does not allow a definite diagnosis of icteric diseases. Therefore, the clinical relevance of serum bilirubin subfractionation by alkaline methanolysis and subsequent thin-layer chromatography (AM-TLC) was evaluated. Esterified bilirubins could be detected and quantitated in all serum samples investigated. The ratio of serum esterified to total bilirubin was 10-28% in 60 healthy adults (mean 17 +/- 5% S.D.), 1-11% in 77 patients with Gilbert's syndrome (mean 6 +/- 2%), and 2 and 3%, respectively, in two patients with Crigler-Najjar disease type II. The difference was highly significant (p less than 0.001) and the overlap was restricted to three of 139 individuals. The ratio of esterified to total bilirubin was similar to that obtained with HPLC when corrected for with a blank run. The absolute concentration of bilirubin esters in serum from Gilbert's syndrome patients was similar to that from healthy controls, but the unconjugated pigment was increased. In patients with chronic haemolysis (n = 9) and chronic persistent hepatitis (n = 12), the hyperbilirubinaemia consisted of a proportional increase of both unconjugated and esterified bilirubin. As such, the ratio of conjugated to total bilirubin was not significantly different from control values. Patients with acute hepatitis during the first (n = 18) and third ('remission') week of the disease (n = 15), liver cirrhosis (n = 34), and extrahepatic cholestasis (n = 20) predominantly showed an increase in bilirubin conjugates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subfractionation of serum bilirubins by alkaline methanolysis and thin-layer chromatography. An aid in the differential diagnosis of icteric diseases. 225 26


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