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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma bile acid concentrations were measured in normal horses. There was no diurnal variation in values, and age and sex had no effect. There was no significant difference between serum and plasma bile acid concentrations in clinically normal horses. Plasma bile acids were stable on storage for one month at -20 degrees C. The total plasma bile acid concentrations together with total and direct bilirubin concentrations and plasma activities of aspartate aminotransferase, glutamate and iditol dehydrogenase were evaluated in horses with various types of hepatobiliary disease (hepatic necrosis, lipidosis, neoplasia and cirrhosis), gastrointestinal disease, cardiovascular, orthopaedic and various other conditions not affecting the liver. Total plasma bile acids together with plasma glutamate and iditol dehydrogenase activities were the best indicators of liver disease. Total plasma bile acid concentrations were the most sensitive indicator of a wide variety of hepatic diseases but alone were unhelpful in differential diagnosis and were of more value when combined with the other tests of hepatic disease.
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PMID:Evaluation of total plasma bile acid concentrations for the diagnosis of hepatobiliary disease in horses. 256 44

In 18 horses there was no effect of age or sex on plasma activities of gamma-glutamyl transferase (gamma-GT), 5'-nucleotidase (5'-NT) and leucine aminopeptidase (LAP). All the enzymes were equally stable after storage for one month at -20 degrees C and there was no significant difference between their activities in serum and plasma in clinically normal horses. The pattern of release of gamma-GT, 5'-NT and LAP into plasma was studied in 114 horses which had a variety of orthopaedic, gastrointestinal, cardiovascular and hepatic (necrosis, lipidosis, neoplasia and cirrhosis) conditions. A definitive diagnosis of hepatic disease was established by histological examination of the liver. gamma-GT and 5'-NT were leaked into plasma in hepatic disease and gamma-GT was the more sensitive indicator of liver damage. There was some evidence that gamma-GT and 5'-NT plasma activities may increase in hepatic necrosis as well as in biliary obstruction. LAP was insensitive and not hepatic specific in the horse.
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PMID:Observations on gamma-glutamyl transferase, 5'-nucleotidase and leucine aminopeptidase activities in the plasma of the horse. 256 9

The diagnostic value of serum gamma-glutamyl transferase (GGT) activity and serum alkaline phosphatase (ALP) activity in the detection of liver disease in the cat (n = 69) was compared. On the basis of histologic examination of the liver, cats were assigned to 8 groups: group 1--complete extrahepatic bile duct obstruction (n = 5), group 2--cholangiohepatitis-cholangitis syndrome (n = 11), group 3--hepatic lipidosis (n = 15), group 4--neoplasia, including lymphosarcoma and myeloproliferative disease (n = 9), group 5--hepatic necrosis (n = 7), group 6--cirrhosis (n = 3), group 7--portosystemic vascular anomaly (n = 4), and group 8--miscellaneous (n = 15). Cats assigned to group 8 lacked substantial histologic abnormalities of the liver. The mean value +/- SD of GGT in 20 clinically normal cats was 0.44 +/- 0.26 IU/L. The highest GGT activity in clinical patients developed in groups 1, 2, and 6. The highest ALP activity developed in groups 1 to 4. Significant correlations between GGT and ALP activities were detected only in groups 2 (P less than 0.001) and 5 (P less than 0.10). Among 54 cats with hepatic disease, only 11% had both the GGT and ALP activities within the normal ranges. Comparatively, 52% had ALP activities within the normal range, and 17% had GGT activities within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnostic value of serum gamma-glutamyl transferase and alkaline phosphatase activities in hepatobiliary disease in the cat. 287 43

The clinical usefulness of measuring serum bile acid concentrations as a diagnostic test for hepatobiliary disease was examined in 80 cats that were suspected of having hepatic disease. Serum values of total bilirubin, alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) also were measured. Fasting serum bile acid values were determined by use of solid-phase radioimmunoassay for total conjugated bile acids or by a direct enzymatic spectrophotometric method. A definitive diagnosis was established by histologic examination of the liver, and on the basis of these findings, cats were assigned to groups (1 to 8, respectively) including: extrahepatic bile duct obstruction, hepatic lipidosis, cirrhosis, intrahepatic cholestasis (cholangiohepatitis, cholangitis), neoplasia, hepatic necrosis, portosystemic vascular anomalies, and miscellaneous. Cats in group 8 had no morphologic evidence of hepatobiliary disease or had hepatic lesions that were mild. Test efficacy of fasting serum bile acids, total bilirubin, ALP, ALT, and AST were expressed by use of 4 indices: sensitivity, specificity, positive predictive value, and negative predictive value. The diagnostic efficacy of fasting serum bile acids was examined alone and in combinations with the other tests. There was wide overlapping of values of fasting serum bile acids, total bilirubin, ALP, ALT, and AST among cats in groups 1 to 7. The specificity of fasting serum bile acids for the diagnosis of hepatic disease exceeded 90% at values greater than or equal to 5 mumol/L and reached 100% at greater than or equal to 15 mumol/L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bile acid concentrations in the diagnosis of hepatobiliary disease in the cat. 377 58

Storage of cholesterol, cholesterol esters, and triglycerides with distribution in different organs is characteristical in 5 distinguishable familiary thesaurismoses. Cholesterol storage disease is due to relatively benign storage of cholesterol esters predominantly in the liver with gross enlargment of this organ. Acid lipase is lysosomes is also nearly inactive in the maligne Wolman's disease with calcification of the adrenals, hepatosplenomegalia and death during infancy by gastrointestinal complications. Very similar are other diseases without renal calcification but partly with pulmonal storage of cholesterol. In only one family another type of cholesterol lipidosis and cirrhosis together with aplasia of gall bladder, renal cysts, and hydronephrosis has been observed. Two types of pure triglyceride storage disease are described, but each of them in only few cases. Tendinous xanthomatosis by storage of cholestanol predominantly in brain with mental retardation, and xanthomatosis with beta-sitosterol but normal mental development are two rare steatoses with abnormal cholesterol-like lipids, in which xanthomatas are visible.
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PMID:[Disease with storage of neutral lipids (author's transl)]. 703 73

Oncogenic agents may hit at least four different types of target cells in the liver, namely the hepatocytes, the cholangiolar cells, the sinusoidal endothelial and the perisinusoidal cells. All of these cell types may give rise to neoplasms which develop from phenotypically altered preneoplastic cell populations via various intermediate stages to benign and/or malignant neoplasms. The manifestation of hepatocellular neoplasms induced by chemicals, radiation or viruses in different species including primates is regularly preceded by focal metabolic and morphological alterations which emerge in the liver parenchyma long before the neoplasms appear. The predominant sequence of metabolic changes leads from a focal excessive storage of glycogen (glycogenosis) through intermediate stages, in which the glycogenosis is frequently replaced by a lipidosis, to glycogen-poor hepatocellular carcinomas. The early hepatocellular glycogenosis is due to a disturbance in glycogen breakdown, which is associated with a dysfunction of signal transduction and glucose transport. During progression from the preneoplastic hepatocellular glycogenosis to glycogen-poor hepatocellular neoplasms a fundamental shift in carbohydrate metabolism takes place, gradually redirecting metabolites such as glucose-6-phosphate toward alternative metabolic pathways such as the pentose phosphate pathway and glycolysis. Studies on about 70 resected or explanted livers from patients bearing hepatocellular carcinomas or suffering from cirrhosis provided evidence for focal changes in glycogen metabolism similar to those observed in laboratory animals. An alternative sequence of cellular changes involving oncocytes and amphophilic cell populations rich in mitochondria and sometimes also peroxisomes has been observed in rats after administration of non-genotoxic hepatocarcinogens, particularly peroxisomal proliferators, and in woodchucks during hepadnaviral hepatocarcinogenesis. Our observations suggest fundamental changes in the cellular energy metabolism during hepatocarcinogenesis, which are most probably due to a disturbance in signal transduction pathways and may be causally linked to neoplastic cell conversion.
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PMID:[Sequential cellular and molecular changes during hepatocarcinogenesis]. 860 Jun 97

In horses with hepatic necrosis, lipidosis, neoplasia and cirrhosis, progression of the disease was studied by serial measurements of total serum bile acid concentrations and of plasma glutamate dehydrogenase (GD) and gamma glutamyl transferase (gamma GT) and by liver biopsy. Plasma ammonia concentrations were significantly elevated compared to clinically normal horses, but such changes were not always accompanied by a decline in plasma urea concentration. A fall in plasma glucose concentration carried a guarded prognosis. These were all invaluable aids in early diagnosis and throughout the disease course. The study suggests that other factors, such as hypokalaemia, alkalosis, short chain volatile fatty acids, false and true neurotransmitters, may be important in the pathogenesis of hepatic coma in the horse.
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PMID:Clinical and pathological studies in horses with hepatic disease. 870 47

Nutritional intake in the patient with hepatobiliary disease provides the cornerstone of balanced medical care. Optimal recommendations require consideration of general nutritional principles, special species requirements and contemporary needs uniquely related to the patient's medical problem. Although general recommendations follow well-established guidelines developed to meet metabolic requirements for normal health, there is little information regarding altered requirements in animals that are ill. Consequently, recommendations for animals have been derived empirically from studies completed in humans, most work having been done in patients with end stage cirrhosis or liver failure complicated by hepatic encephalopathy. This is problematic because most veterinary patients with liver disease are not in hepatic failure and do not suffer from hepatic encephalopathy. Iatrogenic malnutrition can develop in patients when protein-restricted diets are inappropriately recommended. Insufficient energy intake and negative nitrogen balance can complicate a patient's condition, impairing tissue regeneration and recovery from disease. This paper reviews strategies that can be used to individualize nutritional management in small companion animals with hepatobiliary disease. Consideration is given to both the known and controversial issues regarding energy requirements, dietary energy distribution, vitamin and micronutrient supplementation, the special requirements of the cat with hepatic lipidosis, as well as strategies effective for palliation of hepatic encephalopathy.
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PMID:Nutritional support for dogs and cats with hepatobiliary disease. 986 54

The examination of 675 caprine livers from a slaughterhouse in the Greater Muscat area in the Sultanate of Oman revealed that 63 (9.3%) exhibited gross pathological changes leading to condemnation of this organ. Forty of these livers (71.4%) exhibited one major abnormality, whereas the remaining 28.6% had two or more lesions. The most frequently occurring disorder was diffuse hepatic lipidosis (4.0%), followed by bacterial associated abscesses (2.4%), cysticercosis (1.9%), and eosinophilic granulomata (1%). Although the cause for the hepatic lipidosis was not determined it appeared to be a reversible condition based on the absence of degenerative nuclei within the affected hepatocytes. Conditions observed in only a single liver were subcapsular (non-parasitic) cysts, focal necrosis, micronodular cirrhosis, extensive bile duct proliferation and diffuse haemorrhage.
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PMID:An abattoir survey of caprine liver diseases in the sultanate of Oman. 1055 42

Hepatic stellate-cell lipidosis due to hypervitaminosis A can lead to cirrhosis, which can be averted by restricting vitamin A intake. Other causes, including the use of synthetic retinoids, have been postulated. We studied the frequency and etiology of stellate-cell lipidosis in patients undergoing liver biopsy for reasons other than vitamin A abuse. Fourteen cases (1.1%) were identified retrospectively among 1,235 nontransplant liver biopsy specimens examined from January 1995 through December 1999. Diagnostic criteria included the following: lipid-laden cells in the space of Disse; small, dark, crescent-shaped nuclei with inconspicuous nucleoli; and wispy cytoplasmic strands separating fat droplets. Patient details, reason for biopsy, and medication use were studied. Reasons for biopsy included hepatitis C (10 cases), abnormal liver enzyme levels (2 cases), methotrexate use (1 case), and alcohol abuse (1 case). Hypervitaminosis A was not suspected clinically in the 5 patients who used oral vitamin A or 3 who used topical tretinoin (Retin-A). In 6 patients, no cause of stellate-cell lipidosis was discerned. Stellate-cell lipidosis should be reported to alert clinicians to a potentially preventable form of liver injury.
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PMID:Stellate-cell lipidosis in liver biopsy specimens. Recognition and significance. 1257 96


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