Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.109 (AST)
6,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial ketone body ratio (AKBR [acetoacetate/beta-hydroxybutyrate]) was measured in nineteen patients under medical supportive therapy for fulminant hepatic failure (FHF), in order to evaluate its predictive value relative to liver transplantation. Of the 19 patients 8 (42%) were salvaged and 11 (58%) died. Seven of 8 survivors showed an increased AKBR over 0.6 at 24-hr after admission, and all of them showed AKBR over 0.8 at 48-hr with subsequent maintenance of the value over 1.0. By contrast, all 11 nonsurvivors demonstrated sustained suppression of AKBR below 0.4 from 24 to 72 hr after admission. AKBR values at 24 and 48 hr showed statistically significant differences between survivors and nonsurvivors. Neither the grade of portal systemic encephalopathy (PSE) nor other conventional laboratory parameters--such as AST, bilirubin, ammonia, prothrombin time, hepaplastin test, fibrinogen, and platelet count--could discriminate between survivors and nonsurvivors by univariate analysis. These results indicate that AKBR can accurately predict the prognosis of FHF at the initial 24-48 hr after admission, and that it can play an important role in setting the indication of FHF for liver transplantation.
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PMID:Arterial ketone body ratio as a possible indicator for liver transplantation in fulminant hepatic failure. 201 30

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

The levels of endogenous serum digoxin-like immunoreactive substances were investigated during development of encephalopathy in patients with fulminant hepatic failure. The 67 patients studied had varying degrees of hepatic failure as a result of viral hepatitis or paracetamol overdose. Serum levels of digoxin-like immunoreactive substances were significantly increased in both viral hepatitis and paracetamol overdose, with mean values of 0.42 +/- S.D. 0.25 ng per ml (n = 36) and 0.53 +/- 0.19 ng per ml (n = 31), respectively, as compared to normal control subjects with mean values of 0.01 +/- 0.02 ng per ml (n = 21, p less than 0.001). A statistically significant correlation was found between serum digoxin-like immunoreactive substances and the degree of encephalopathy in the viral hepatitis patients and with the serum creatinine in the paracetamol overdose patients where renal failure was more severe. No correlation was found with liver damage as assessed by the prolongation of the prothrombin time, serum AST or bilirubin values. Experiments with ultrafiltration and heating showed that both free nonprotein-bound digoxin-like immunoreactive substances and the total digoxin-like immunoreactive substances measured were increased. Column chromatography of ultrafiltrates of fulminant hepatic failure serum on Sephadex G-25 demonstrated at least two peaks with digoxin-like immunoreactive activity. Reduced renal function is an important factor in the increased serum level of digoxin-like digoxin-like immunoreactive substances, but their presence due to liver failure, where there is increased permeability of the blood-brain barrier, could be relevant to the development of hepatic encephalopathy.
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PMID:Digoxin-like immunoreactive substances in severe acute liver disease due to viral hepatitis and paracetamol overdose. 282 15

One hundred and thirty-one patients underwent clinical and biological investigation with the following determinations performed on the same day; presence or absence of ascites, icterus and/or encephalopathy, coagulation study, biochemical determinations including albumin, transferrin and immunoglobulins immunoassays. The principal component analysis of biological data showed two sets of highly representative and inversely correlated data; one included coagulation tests, albumin and transferrin, and the other included immunoglobulin A/transferrin ratio, immunoglobulin A and total bilirubin. Clinical and biological data were computed using discriminant analysis between dead and survivors. Six parameters were then selected (total bilirubin, encephalopathy, factor V, AST, antithrombin III and transferrin) giving a correct prognosis in 81.6% (31/38) of cases in a test sample. Neither ascites nor immunoglobulins were useful for the estimation of the prognosis.
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PMID:Multivariate analysis of clinical and biological data in cirrhotic patients: application to prognosis. 679 41

Twelve serologically proven cases of non-A, non-B (NANB) hepatitis have been described. The clinical course was mild in 11 patients. One patient, however, presented in portal systemic encephalopathy and required steroid treatment. Nine of the 12 patients continued to exhibit raised transaminase (AST) activities six or more months after the onset of the acute hepatitis. In these immunoglobulin concentrations were normal and autoantibodies were not present in significant titre. Four patients had evidence of previous hepatitis B infection, suggesting that the route of transmission of NANB might be similar to that of hepatitis B virus. A further four patients gave a history which suggests a possible parenteral mode of transmission. Liver biopsies were carried out both in the acute (8 cases) and chronic (6 cases) phases of the disease. Histological findings in liver biopsies covered the whole spectrum of acute and chronic hepatitis and 1 patient had cirrhosis. One notable feature in these biopsies was the presence of fatty changes.
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PMID:Clinical and histological features of a group of patients with sporadic non-A, non-B hepatitis. 679 15

The risk for developing acute liver failure after halothane exposition was calculated between 1:8,000 and 1:36,000. The case report given on a 22 year old man with halothane-induced hepatic failure is unusual, because the typical risk factors as age over 40, female sex, obesity, and previous exposure to halothane were not present. Two days after exposure to halothane the patient suffered acute liver failure with severe coagulopathy (factor V = 5% activity), and encephalopathy grade IV complicated by renal failure and respiratory insufficiency. Maximal increases of enzymes in blood were AST 3900 U/L, ALT 2570 U/L, LDH 10600 U/L. After six days the patient underwent liver transplantation with complete anuria and instable circulation. Explanted liver showed massive necrosis (70% of parenchyma) and fatty changes. The liver transplant had immediately a good function and renal failure resolved within three days. In the follow-up of 3 1/2 years the patient suffered no further complications. Culturing the patient's lymphocytes in the lymphocyte transformation test a strong reaction could be detected with a stimulatory index of 20. Maximal proliferation was observed when lymphocytes were incubated with plasma metabolites of a volunteer drawn 120 minutes after anesthesia with halothane was started.
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PMID:[Liver transplantation in halothane-induced liver necrosis]. 802 96

Recent experience suggests that a diagnosis of Reye's syndrome based on clinical and biochemical grounds alone may be unreliable. Two patients are presented here, whose clinical manifestation suggested Reye's syndrome. The biochemistry data were also compatible with Reye's syndrome except that the levels of serum AST and ALT were significantly higher with normal serum ammonia level. Blood amino acid and urinary organic acid assay all showed negative findings. Histological findings of the liver showed marked centrilobular necrosis rather than fatty metamorphosis. The muscle biopsies did not show lipid accumulation in the muscle fibers as well. The findings in our patients suggested that a confirmatory diagnosis of Reye's syndrome requires a characteristic pathological findings of the liver in order to differentiate Reye's syndrome from Reye-like syndrome, especially acute encephalopathy associated with centrilobular necrosis of the liver.
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PMID:[Acute encephalopathy associated with centrilobular necrosis of liver mimicking Reye's syndrome--report of two cases]. 838 58

To evaluate the hepatic regenerative response in patients with alcoholic liver disease, sera from 263 patients with severe alcoholic hepatitis and/or cirrhosis were analyzed for hepatocyte growth factor (HGF) and alpha-fetoprotein (AFP). HGF concentration was elevated above healthy controls in 95% of the patients (median level = 2.4 ng/ml), whereas AFP tended to be depressed below controls (median level = 4.1 ng/ml). Correlations with parameters of liver injury (i.e., ascites, encephalopathy, AST bilirubin, and protime) all showed a more significant correlation with HGF concentrations than those of AFP. Patients with HGF levels below the mean (4 ng/ml) exhibited significantly better survival (median survival = 35 months vs. 8.5 months for those with HGF > or = 4 ng/ml; p = 0.007). Serum HGF levels were associated with various specific histologic features of alcoholic hepatitis that included, but were not exclusively related to, necrosis.
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PMID:Human hepatocyte growth factor in alcoholic liver disease: a comparison with change in alpha-fetoprotein. Department of Veterans Affairs Cooperative Study Group 275. 898 14

The impact of dengue haemorrhagic fever (DHF) on liver function was studied by measuring serum transaminase levels on 45 patients with DHF confirmed by virus isolation and serodiagnosis in 1995. Abnormal levels of AST and ALT were observed in 97.7 and 37.3% of the patients, respectively. The fact that the level of AST was higher than that of ALT and that the elevation of transaminases was mild to moderate in most cases (< 5-fold greater than the normal upper limit for AST and ALT) showed that liver involvement was also mild to moderate in most cases of DHF. The results of transaminases did not differ significantly between cases with and without hepatitis B or hepatitis C virus infection, nor between primary and secondary cases of infection, but a significantly higher elevation of AST and ALT was observed in DHF patients with gastrointestinal haemorrhage. Two patients with dengue encephalopathy (in 1992) and one patient with dengue encephalopathy who died of massive gastrointestinal haemorrhage (in 1995) had unusually high transaminase levels as a sign of acute liver failure. It is concluded that DHF may cause mild to moderate liver dysfunction in most cases; only some patients may suffer from acute liver failure leading to encephalopathy and death.
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PMID:The impact of dengue haemorrhagic fever on liver function. 927 78

The findings on magnetic resonance imaging (MRI) or computed tomographic scan in 35 children with acute encephalopathy (AE) induced by infections were categorized into five groups: (1) normal findings (11 cases), (2) normal findings in the acute phase followed by mild brain atrophy (1 case), (3) severe brain edema which developed within 48 hours after the onset of AE (7 cases), (4) diffuse cortical necrosis which appeared around 4 days after the onset of AE (9 cases), and (5) symmetric thalamic lesions (7 cases). Their outcomes were as follows: three cases developed epilepsy in (1) and (2); six died and one had a sequel of severe brain damage (SBD) in (3); all cases survived but had SBD in (4), and four died, one had SBD, and 2 recovered in (5). Serum AST were elevated in 7.7 and 6 cases in (3), (4) and (5), respectively. In all of them, there were more than one case having liver histologies consistent with Reye syndrome.
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PMID:[Clinical studies on 35 patients with infection-related acute encephalopathy]. 961 58


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