Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 131 patients on a medical service and 97 patients on a surgical service, in whom a diagnosis of hepatobiliary disease was verified in the hospital, the diagnostic value of routine liver tests performed soon after admission was evaluated by stepwise discriminant analysis. By measurements of alanine aminotransferase, alkaline phosphatases, gamma globulin, prothrombin time, bilirubin, and albumin, half of the medical patients were correctly classified into one of seven diagnostic categories. Aminotransferase contributed most to the classification, being twice as effective as random allocation. Decreasing the number of diagnostic categories to three (hepatitis, fatty liver, and chronic liver disease) increased the frequency of correct allocation to 80%. The allocation of all the patients to seven medical and four surgical diagnostic categories by means of four tests (aminotransferase, alkaline phosphatases, prothrombin time, and bilirubin) was significantly improved by each step with a misclassification rate of 55% when all tests were used. A reduction of the diagnostic groups to five (hepatitis, fatty liver, chronic liver disease, duct obstruction and tumor) increased the frequency of correct allocation to 63%. The analysis demonstrates the limited diagnostic effectiveness of routine liver tests when used alone. The absolute discrimination values depend on the a priori frequencies of the diagnostic groups investigated, and therefore may vary from time to time and from place to place.
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PMID:Diagnostic value of routine liver tests. 4 96

In 9 patients with radiolucent gallstones, percutanous liver biopsy was performed during treatment with chenodeoxycholic acid in a dose of 500 to 750 mg per day for 3-14 months. In 4 patients pretreatment specimens were available for comparison. No sign of hepatic cellular necrosis or bile duct proliferation was noticed in the biopsies. In 2 patients hepatic steatosis was reduced, and in one patient moderate portal tract inflammation decreased during therapy. Mean values of alkaline phosphatases, alanine aminotransferases, prothrombin, and serum lipids remained unchanged and did not exceed normal limits. In 5 patients the urinary bile acid profile was examined during therapy. Chenodeoxycholic acid constituted 27-50%, lithocholic acid 25-63%, and ursodeoxycholic acid 0-13% of total bile acids in urine. The renal excretion of total bile acids was estimated to be less than two mg per day in each patient. From 86 to 100 per cent of the bile acids in urine was sulfated.
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PMID:Hepatic morphology and bile acid composition of bile and urine during chenodeoxycholic acid therapy for radiolucent gallstones. 93 99

The levels of C3, cholinesterase, albumin and prothrombin were determined in 46 patients (27 males and 19 females) - 26 with cirrhosis of the liver, 9 with acute hepatitis, 6 with chronic aggressive hepatitis, 1 with chronic persistent hepatitis and 4 with fatty liver. In all patients and, particularly in those with cirrhotic liver, it was shown that the normal or pathological level of serum C 3 is related both qualitatively and quantitatively to the normal or pathological levels of cholinesterase, albumin, and prothrombin. The percentage in which the levels of these four parameters were pathological was considerably higher in the cases with hepatic coma than in the cases without hepatic coma. The determination of the range of confidence for the 4 parameters showed that, in the patients with hepatic coma, cholinesterase reacted most sensitively to liver damage (0.5 - 0.94) followed by C3 and prothrombin (0.33 - 0.81). Also in the cases without hepatic coma, cholinesterase was the most sensitive indicator (0.05 - 0.29), followed by prothrombin (0.03 - 0.24), albumin and C3 (0.00-0.16).
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PMID:Serum levels of C3 and cholinesterase in various diseases of the liver. 125 98

Serum level of osteocalcin (OC) is believed to be a specific biochemical parameter of bone formation. Decreased serum OC has been reported in alcohol-intoxicated subjects, in patients with primary biliary cirrhosis and in patients with chronic alcoholic liver disease. The question was, whether lower OC level could be detected in patients with nonalcoholic and non-cholestatic chronic liver disease. The serum OC was measured by RIA developed in our laboratory. Results were compared to age and sex matched controls. Decreased OC level was found in 35 out of 47 (74%) patients with non-alcoholic and non-cholestatic liver disease as chronic persistent hepatitis, chronic active hepatitis, fatty liver and cirrhosis, in 21 out of 26 (80%) patients with alcoholic liver disease and in 8 out of 15 (53%) primary biliary cirrhosis. None of the patients had elevated value. There was no correlation between the decreased OC level and the duration or severity of the liver disease and the laboratory parameters as bilirubin, AST, ALT, alkaline phosphatase, albumin, prothrombin, and serum 25-OH-D3 vitamin level. Decreased OC was found also in the patients without cirrhosis. The possible causes are discussed. Relying upon these findings it is supposed that chronic liver disease by itself can influence the osteoblast activity also by some unknown mechanism.
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PMID:[Decreased serum osteocalcin level in non-alcoholic and alcoholic chronic liver diseases]. 185 6

Two hundred eighty-one alcoholic patients were prospectively evaluated by clinical, biochemical, and histologic parameters during a 4-yr period to assess their prognosis. They were stratified into four categories of injury: 1) fatty liver (26 patients), 2) acute alcoholic hepatitis (106), 3) cirrhosis (39), and 4) cirrhosis with superimposed alcoholic hepatitis (111). The rate of survival and variables correlating with survival varied according to the group. At 48 months, 70% of the patients with fatty liver were alive, 58% in the alcoholic hepatitis group, 49% in cirrhosis, and 35% in alcoholic hepatitis superimposed upon cirrhosis. Within group one, deaths were due to causes unrelated to liver disease. In the alcoholic hepatitis group, factors significantly correlating with survival were ascites, alanine amino-transferase levels, grams of alcohol consumed, continuation of alcohol intake, and clinical severity of disease. Survival in patients of group three correlated significantly with prothrombin time and histologic severity score. Patients with combined cirrhosis and alcoholic hepatitis exhibited the worst prognosis, with the most significant predictors of survival being age, grams of alcohol consumed, the ratio of serum aminotransferases (AST:ALT) and the histologic and clinical severity of the disease. Although a different pattern of correlates was observed for each pathologic level of injury, knowledge of the various correlates aids in prognostic assessment.
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PMID:Prognostic factors in alcoholic liver disease. VA Cooperative Study Group. 199 35

Plasma endotoxin concentration was measured in 85 patients with alcoholic liver disease (alcoholic cirrhosis (n = 64), alcoholic hepatitis without cirrhosis (n = 11), fatty liver (n = 10), and in patients with non-alcoholic cirrhosis (n = 15]. Endotoxin concentration was determined with an improved chromogenic substrate assay, using individual standard curves for each plasma sample. In patients with alcoholic cirrhosis the mean endotoxin concentration was significantly higher than in patients with non-alcoholic cirrhosis (p less than 0.05). In addition, distinctly higher endotoxin concentrations (greater than 20 pg/ml) were more frequently observed in patients with alcoholic cirrhosis than in non-alcoholic cirrhosis (34.4 vs. 14.3%, p less than 0.05). Mean endotoxin concentration was not significantly higher in cirrhotics with ascites or esophageal varices as compared with the subgroup without ascites or esophageal varices. The endotoxin concentration did not correlate with serum bilirubin, prothrombin concentration or serum enzyme activities. In patients with alcoholic liver disease, however, endotoxin concentration revealed a negative correlation (p less than 0.05) with the concentration of high density lipoprotein cholesterol. On admission endotoxin concentrations in alcoholics with fatty liver were similarly elevated as observed in alcoholic cirrhosis. In six out of 12 patients with fatty liver or alcoholic hepatitis, in whom a second sample of plasma was investigated after 6 to 8 days, endotoxemia was no longer detectable; in the remaining patients, the endotoxin concentration decreased markedly. The results indicate that, irrespective of the stage of liver disease, alcohol abuse favours the development of endotoxemia. They support the hypothesis that gut-derived endotoxins might play a role in the initiation and aggravation of alcohol-induced liver disease.
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PMID:Plasma endotoxin concentrations in patients with alcoholic and non-alcoholic liver disease: reevaluation with an improved chromogenic assay. 205 Sep 95

24 patients with alcoholic intake were classified according to the amount of alcohol ingestion; clinical symptoms and signs, liver function tests (bilirubin, aminotransferases and prothrombin time) were analyzed. In all patients a percutaneous liver biopsy was performed and tissue stained by hematoxylin-eosin, wilder reticulin and Mallory trichromic. 9 Histologic criteria were analyzed. 4 groups according to the histology were identified. Group 1 (5 patients) hepatic fibrosis and/or fatty liver. Group 2 (5 patients) alcoholic hepatitis. Group 3 (10 patients) cirrhosis. Group 4 (4 patients) normal. 20% of patients with fatty liver, 80% of alcoholic hepatitis and 100% of cirrhotics referred ingestion or more than 160 g of ethanol and important correlation between liver histological damage and alcohol ingestion. Telangiectasia was the most common clinical finding and present in all hepatitis, 70% of cirrhotics and only 20% of fatty livers. Hemosiderosis was found in 60% of cirrhotics and in alcoholic hepatitis. Only 40% of patients with fatty liver and inflammatory cells while this was evident in all patients with alcoholic hepatitis and those with cirrhosis. Mallory bodies were identified in only 20% of cirrhotics and in none of the alcoholic hepatitis. The results suggest that there are significant differences from a histological and clinical point of view that distinguish alcoholic liver disease as seen in Venezuela from that reported in other countries.
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PMID:[Alcoholic liver disease in Venezuela. Clinical hepato-functional and histopathologic course]. 215 50

A previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.
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PMID:Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation. 240 63

Reye's syndrome (RS) is generally considered a childhood disease. We report our experience with RS in adults in the metropolitan Milwaukee area. Reye's syndrome was diagnosed in seven 18- to 46-year-old adults. The diagnostic criteria were as follows: viral prodrome followed by vomiting and encephalopathy without focal neurological signs, normal cerebrospinal fluid values, increased levels of serum aminotransferases (transaminase), prolonged prothrombin time, elevated blood ammonia levels, and characteristic microvesicular fatty liver and mitochondrial changes. None of the patients was hypoglycemic. The diagnosis of RS was entertained in 22 but confirmed in only seven patients. In cases of non-Reye's encephalopathy, drug ingestion presented as one of the most difficult differential diagnostic problems, which also included alcohol abuse, collagen vascular disease, and hepatitis B surface antigenemia. Clinical jaundice, distinctly uncommon in RS, was present in only one patient who presented to us in stage V coma. In adults, RS is more difficult to diagnose and should be suspected more frequently in patients with unexplained altered behavior following a viral illness and vomiting. Liver biopsy can be performed safely and is usually mandatory in adults. Patients with RS diagnosed during stage I or II coma and treated experienced an uneventful recovery.
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PMID:Reye's syndrome in adults. Diagnostic considerations. 380 May 31

Five patients had amiodarone hepatotoxicity detected on routine biochemical monitoring. Symptoms attributable to hepatotoxicity were minimal or absent; reversible hepatomegaly was seen in two patients, whereas three patients had signs of nonhepatic amiodarone toxicity before or with hepatotoxicity. Serum aminotransferase levels were elevated in all patients and alkaline phosphatase levels in four; no patient had hyperbilirubinemia or prolongation of the prothrombin time. Light microscopy showed steatosis, cellular degeneration, and cellular necrosis in the biopsy samples of four patients, whereas the fifth patient's sample had a granulomatous injury pattern. Electron microscopic study of liver tissue done in two patients showed phospholipid-laden lysosomal lamellar bodies. These findings suggest that both toxic and hypersensitivity liver injury can occur in response to amiodarone. The presence of phospholipid-laden lysosomal lamellar bodies may help differentiate amiodarone hepatotoxicity from alcoholic liver disease or other causes of hepatic steatosis.
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PMID:Amiodarone hepatotoxicity. A clinicopathologic study of five patients. 394 78


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