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)

The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.
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PMID:Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989). 174 13

Sulfobromophthalein dye test and galactose tolerance test were performed, using both substances simultaneous i.v. injection, in 48 subjects with chronic persistent hepatitis, chronic active hepatitis and liver cirrhosis (with and without ascites). As control group 10 normal subjects were tested. Sulfobromophthalein excretion constant ( K1BSF ) drawn from the first part of the retention curve, and the galactose excretion constant (K Gal) were considered. The following conclusions were obtained: a) K1 BSF and K Gal are well-correlated; b) K1 BSF appears more sensitive for a whole evaluation of liver involvement, in absence of evident jaundice (total serum bilirubin less than 6 mg/100 ml); c) K Gal is less reliable in presence of ascites because of the artificial increase in galactose plasmatic clearance provoked by the substance passage to the effusion fluid; d) the statistical analysis using discrimining function methods makes possible a better distinction among the various kinds of liver diseases; e) the same type of statistical analysis shows a difference between cirrhotics with ascites responding to medical therapy in comparison to treatment- resistent ascites. This fact may account for a different level of hepatic functional activity.
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PMID:[Clinico-statistical evaluation of the simultaneous clearance of sulfobromophthalein and galactose in chronic liver diseases]. 667 75

Advanced chronic hepatic disease was observed in 5 dogs that had received anticonvulsant drug therapy for 2 to 3 years. Clinical signs included anorexia, weakness, and restlessness, and 2 dogs also had ascites. There were remarkable increases in the serum activities of alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase. The total serum bile acid concentration was high in 3 of 4 dogs that were tested. Sulfobromophthalein excretion was delayed in all dogs. Histologic examination of liver specimens from 4 of the dogs demonstrated macronodular or micronodular cirrhosis.
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PMID:Hepatic cirrhosis associated with long-term anticonvulsant drug therapy in dogs. 711 8

Fasting and postprandial serum concentrations of conjugates of cholic (CCA) and chenodeoxycholic (CCDA) acid measured by radioimmunoassay were compared with morphological changes in percutaneous liver biopsies from 49 patients with alcohol abuse. Sulfobromophthalein (BSP) and galactose elimination tests were also performed, and serum levels of aminotransferases (ASAT, ALAT), glutamyltransferase, alkaline phosphatase, and bilirubin were determined. Raised fasting serum concentrations of CCDA were found in 29 patients (59%), whereas elevated fasting serum levels of CCA were found in 19 patients (39%). The mean fasting and postprandial serum bile acid concentrations were significantly higher in patients with hepatofibrosis and cirrhosis than in those with only fatty changes. The extent of the postprandial rise, however, was variable and not significantly different among the various groups. The BSP elimination test was abnormal in 12 patients (25%) but gave normal results in 2 of the 3 patients with cirrhosis of the liver. The galactose elimination rates differed only between patients with normal liver biopsies and patients with cirrhosis of the liver. The serum enzyme levels were not significantly different between the various morphological groups. It is concluded that determinations of fasting serum bile acids, especially CCDA, give more reliable and sensitive information on the degree of liver damage in alcoholic liver disease than BSP and galactose elimination tests or serum enzyme assays.
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PMID:Serum cholic and chenodeoxycholic acid conjugates and standard liver function tests in various morphological stages of alcoholic liver disease. 720 76