Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of 18 chronic alcoholic patients who had sclerosing hyaline necrosis in noncirrhotic livers was compared with a group of 12 similar individuals with acute alcoholic hepatitis, but no centrilobular fibrosis. In cases with sclerosing hyaline necrosis, the most characteristic features were portal hypertension with very large, tender livers and unusually high glutamic-oxalacetic transaminase values; these were associated with centrilobular fibrosis and abundant alcoholic hyalin. Three of these patients died within two years and in two of these, early cirrhosis was found at necropsy. In the cases of acute alcoholic hepatitis, hepatomegaly was the most conspicuous finding, and only a single patient died; death here was unrelated to hepatic disease, the liver being unremarkable at necropsy. Patients who had sclerosing hyaline necrosis tended to remain ill for significantly longer periods. These observations, in conjunction with evidence gathered from the literature, seem to suggest that sclerosing hyaline necrosis is an obligatory step in the natural evolution of alcoholic hepatic disease, especially in cases that evolve into cirrhosis.
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PMID:Sclerosing hyaline necrosis in noncirrhotic chronic alcoholic hepatitis. 6 9

The present study reported a group of 168 chronically alcoholic patients with a daily ingestion superior to 80 grams. Twenty of these patients (10 percent) did not have liver disease, and 148 (68.5 percent) had different forms of liver disease classified by histopathologic examination. Considering a 97 fi MCV as macrocytosis, we have found in the group of alcoholics without hepatopathy a 50 percent rate of macrocythemia with a mean value of 97.9 fl. In the group of chronic alcoholics with liver disease there was a 64.2 percent macrocytosis with a mean value of 100 fl. We have also studied 43 (21.5 percent) patients with cryptogenetic cirrhosis with a 32.6 percent macrocytosis and a mean value of 93.9 fl. With respect to the alcoholic hepatopathy subgroups, macrocytosis is more frequent in portal fibrosis and acute alcoholic hepatitis, the mean value being higher in the latter. We consider macrocytosis to be frequent among alcoholics, and a good persistence indicator of alcoholic ingestion, pathogenically linked to the now proven dyserythropoietic factor of the alcohol upon the bone marrow. There is no statistically significant correlation between anemia and reticulocytes. We consider macrocytosis to be a more precocious data, and believe that the positive correlation with certain intraerythrocitary enzymes in the juvenile population of red cells corroborates this fact. With respect to the rest of parameters studied there was a correlation with gammaglutamiltranspeptidase, glutamic-oxalacetic transaminase, and the value of prothrombin. The values of mean macrocytosis and elevations of gammaglutamiltranspeptidase and glutamic-oxalacetic transaminase are good persistence indicators of alcoholic ingestion.
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PMID:[Macrocytosis in chronic alcoholism (author's transl)]. 52 26

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

Colchicine treatment was used in this randomized placebo-controlled trial in patients with severe acute alcoholic hepatitis [serum bilirubin greater than or equal to 5 mg/dL (85.5 mumol/L) mean, 17.5 +/- 7.5 mg/dL (299.25 +/- 128.25 mumol/L)]. Hospitalization mortality and morbidity and the effect on biochemical test results were the end points of the treatment. Patients in the two groups were evenly matched by demographics and laboratory test results. Mean time to study entry was less than 7 days from admission. The duration of the trial was 30 days. Thirty-six patients (24 men, 12 women) received colchicine (1 mg orally every morning) and 36 (25 men, 11 women) received an identical placebo. Seven (19%) colchicine-treated and six (17%) control patients died during the index hospitalization after a mean of 17.4 +/- 10.8 and 17.8 +/- 5.3 days, respectively (NS). During a 4-month follow-up period from entry into the trial, there were two additional deaths in each group. No differences between placebo- and colchicine-treated patients were observed in any of the laboratory parameters (serum bilirubin, aspartate transaminase, alanine transaminase, prothrombin activity, albumin, white blood cell count, hemoglobin, and creatinine) that were followed up over the 30-day treatment period. The frequency of complications did not differ statistically between the two groups. This study showed no effect of colchicine treatment on mortality and morbidity of severe alcoholic hepatitis. Colchicine cannot be recommended for the treatment of patients with alcoholic hepatitis.
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PMID:Failure of colchicine to improve short-term survival in patients with alcoholic hepatitis. 219 90

Altogether 108 patients with acute alcoholic hepatitis (AAH) were examined. Of these, 14 patients (13%) presented with the cholestatic pattern of AAH, 45 with extrahepatic cholestasis, and 45 were healthy. As compared with the total patients' group with AAH, the patients with the cholestatic form consumed alcohol in greater amounts. Due to intensive jaundice, 50% of the patients were admitted by error to the infectious clinic and 32% to the surgical one. The disease runs a comparatively grave course, the general conditions gets deteriorated, the body temperature rises, the patient senses pains in the right hypochondrium, skin pruritus is lacking. As compared with other patterns of cholestasis, cholestatic AAH is characterized by a higher thymol test, higher levels of cholesterol, low density lipoproteins, activation of gamma-glutamyl transpeptidase and aspartate aminotransferase and by a lower level of leukocytes, bilirubin, free fatty acids and alkaline phosphatase. Verification of the diagnosis demands the use of certain up-to-date instrumental methods. To identify the cause of cholestasis, great diagnostic significance is attached to echography.
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PMID:[Clinico-laboratory characteristics of the cholestatic form of acute alcoholic hepatitis]. 263 92

Twenty-eight patients with biopsy or clinical acute alcoholic hepatitis were prospectively randomized to 21 days of conventional therapy (14 control patients) or, in addition, to 2 L/day of a peripheral iv infusion of a 900 mosmol amino acid-glucose solution (14 patients). Cirrhosis was present in 64% of controls and in 54% of infused patients. There were three deaths in controls and one in the infused group. There were no significant intergroup differences in mortality, clinical findings, liver tests, or functional mass by the galactose elimination capacity either at entry or after completion of the study. In controls, there was intragroup improvement in serum bilirubin (p = 0.033) and AST (p = 0.008) but not in other "liver tests" or in functional hepatic mass by galactose elimination capacity. In infused patients there was improvement in bilirubin (p = 0.001), AST (p = 0.008), and serum albumin (p = 0.016). Improvement in functional mass by galactose elimination capacity was significant at the p = 0.052 level. Hyaline was initially present in six of eight pairs of biopsies in both groups. After treatment, five of six pairs in controls but only one of six pairs in the infused group still had hyaline (p = 0.03). This latter finding, if confirmed in larger groups, may be of considerable clinical importance. It is suggested that 3- to 4-wk trials of such protocols may require a longer duration of follow-up in greater numbers of patients to detect important advantages of amino acid-glucose infusions which are only implicit in these findings.
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PMID:A prospective randomized clinical trial of peripheral amino acid-glucose supplementation in acute alcoholic hepatitis. 330 90

A randomized, single-blind controlled multicenter study of insulin and glucagon infusion was carried out in 66 patients with acute alcoholic hepatitis. Thirty-three patients were treated with insulin 10 U and glucagon 1 mg in 500 ml 5% glucose in water via a peripheral vein for 2-6 h three times every day for 3 weeks. Patients in the control group received 5% glucose in an identical fashion. Fourteen control patients and five treated patients died from liver failure during the study (P less than 0.02). Clinical features of liver disease on entry into the study were similar in the two groups, but the total serum bilirubin, aspartate aminotransferase, gamma-glutamyltranspeptidase activities and prothrombin time significantly improved in the treated patients (P less than 0.05). Insulin and glucagon infusion appears to be a promising treatment of acute alcoholic hepatitis.
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PMID:A prospective multicenter study of insulin and glucagon infusion therapy in acute alcoholic hepatitis. 332 Jan 81

To investigate whether complement pathway activation contributes to the clinical and histological features of acute alcoholic hepatitis, we studied the activation of the classical and alternative pathways in patients with alcoholic hepatitis (n = 20), inactive alcoholic cirrhosis (n = 8), heavy drinkers without alcoholic liver disease (n = 10), patients with liver disease of nonalcoholic etiology (n = 11), and healthy control subjects (n = 18). Complement activation was evaluated in the alcoholic hepatitis patients by its correlation with a number of clinical and laboratory features indicative of the severity of liver injury, as well as by comparison of the patient groups. There was no significant difference in circulating C3 [1.02 g/liter, confidence interval (CI) = 0.76-1.28] or C4 (0.25 g/liter, CI = 0.17-0.33) in patients with alcoholic hepatitis when compared with the four control groups. Factor B levels (0.24 g/liter, CI = 0.21-0.27) were higher in the alcoholic hepatitis patients than the control groups (p < 0.01). However, activation of complement (given by the ratios C3d/C3, C4d/C4, and Ba/factor B) was not different in alcoholic hepatitis patients when compared with the control groups. Univariate analysis of a wide range of clinical and laboratory features in the alcoholic hepatitis subjects showed a positive correlation between plasma C3 and serum alkaline phosphatase (r = 0.68, p = 0.0014), AST (r = 0.55, p = 0.015), and gamma-glutamyltranspeptidase (r = 0.47, p = 0.035), but no correlation with clinical or laboratory features associated with high morbidity or mortality. There is no relationship between clinical or laboratory indicators of disease severity and complement activation, and it is unlikely that complement activation contributes to the clinical and histological features of alcoholic liver disease.
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PMID:Lack of plasma complement activation in severe acute alcoholic hepatitis. 874 23

Chronic alcohol related liver disease is characterized by a cascade of events defined as follows: steatosis, steatohepatitis/steatofibrosi, cirrhosis and hepatocellular carcinoma. On one of these histologic patterns may overlap acute alcoholic hepatitis (AAE) (mild, moderate, severe). Severe AAE can cause a severe clinical picture: jaundice with a duration of less than three months, jaundice in the first decompensation event, serum bilirubin higher than 5 mg/dL, ratio AST/ALT >2:1, AST less than 500 IU/L ALT <300 IU/L, neutrophil leukocytosis and increased GGT. In addition, it is possible the presence of encephalopathy, fever, fatigue, coagulopathy. The onset can also be characterized by portal hypertension-related complications. An extremely severe clinical condition is the superposition of an acute insult to a chronic framework, not necessarily a cirrhotic one. This condition has been termed acute on chronic (acute on chronic liver failure - ACLF:), and it is possible to have a SIRS (systemic inflammation response syndrome) with a multi-organ system involvement. The diagnosis, in selected cases, can be confirmed by a transjugular biopsy that allows to reach a histologic prognostic stratification. Several indices are used for the assessment of prognosis and in particular the MDF and the MELD. In our clinical practice we use the MELD. In case of ACLF, the consortium organ failure score (CLIF-C OFS) is used. The therapy is characterized by alcohol abstention, and, in severe forms (MDF >32 and MELD >21) with absence of contraindications, it is possible to use steroids therapy. If a positive answers cannot be obtained, an early liver transplantation is proposed. This possibility, after a careful selection, now is promoted by several authors.
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PMID:[Acute alcoholic hepatitis.] 2890 45

Severe acute alcoholic hepatitis (AAH) can lead to a clinical picture with a six-month mortality rate in more than 70% of cases. This clinical picture is characterized by: jaundice with a duration of less than three months, jaundice at the first failure event, serum bilirubin greater than 5 mg/dL, ratio AST/ALT>2/1, AST less than 500 IU/L, ALT<300 IU/L, neutrophil leukocytosis and a GGT increase. In addition, encephalopathy, fever, asthenia and coagulopathy may be present. Its onset may also be characterized by portal-hypertension-related complications, particularly bleeding and hepato-renal syndrome. In cases where there is an overlapping of an acute form characterized by an etiological factor other than that of the base hepatopathy, acute on chronic liver failure (ACLF) is obtained. This can result in systemic inflammation response syndrome (SIRS) with a multi-organ systemic involvement. Several indices are used to evaluate the prognosis, in particular Maddrey's discriminant function (mDF) and the model of end stage liver disease (MELD). In our clinical practice, we use the MELD routinely. In cases of ACLF, a consortium organ failure score (CLIF-COFs) is used. Therapy is characterized by abstention in cases of severe forms (mDF>32 and MELD>21); in the absence of contraindications, steroid therapy is possible. In cases of an unresponsive liver, transplantation is premature. In our view, this possibility, after proper selection, must be offered for both prognostic and ethical reasons.
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PMID:Acute alcoholic hepatitis: a literature review and proposal of treatment. 2911 98


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