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)

The prevalence of delta coinfection in course of acute B hepatitis has been studied in two periods (September-November 1984: 51 cases; April-June 1985: 50 cases). The prevalence resulted of 37.2% in the first period and of 48% in the second, without a statistically significant increase. Delta coinfection did not show greater severity, as evaluated by the levels of AST, ALT, total bilirubin and prothrombin activity, than hepatitis B not coinfected. The only factor of risk statistically significant for the acquisition of delta coinfection was i.v. drug abuse.
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PMID:[Delta co-infection: prevalence, severity and association with risk factors]. 382 88

Ninety-six liver cirrhosis patients with bleeding esophageal varices receiving long-term sclerotherapy with the flexible endoscope were studied prospectively to analyze mortality and rebleeding risk factors. The difference in the 1-year survival rates of Child's groups A (100%) and B (82%) versus Child's C patients (38%) was highly significant (p less than 0.001). Multivariate analysis revealed that, as single factors, serum bilirubin, grade of ascites, and prothrombin time and, as a combination, the four variables bilirubin, ascites, aspartate aminotransferase, and age distinguished best between survivors and non-survivors during the first 6 months after inclusion in the study. For the separation of rebleeders and non-rebleeders during the first 2 months, prothrombin time and grade of ascites gave the best distinction. Thus, cirrhotics with variceal hemorrhage, ascites, jaundice, and a prolonged prothrombin time remain a high-risk group also with long-term sclerotherapy.
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PMID:Long-term sclerotherapy of bleeding esophageal varices in patients with liver cirrhosis. An evaluation of mortality and rebleeding risk factors. 387 6

T-2 toxin was given as a single intravascular dose at either 0.6 or 4.8 mg/kg to different groups of 50-kg female swine. Blood samples were taken at hourly intervals for determination of concentrations or activities of the following substances in serum or plasma: creatinine, blood urea nitrogen, inorganic phosphorus, total calcium, ultrafilterable calcium, magnesium, sodium, potassium, chloride, total protein, albumin, cholesterol, glucose, alkaline phosphatase, aspartate aminotransferase, and total bilirubin. Coagulation analyses included prothrombin time, partial thromboplastin time, activated coagulation time, and fibrin degradation products. Red blood cell, white blood cell, and platelet counts, hemoglobin concentrations, and hematocrits were determined from whole blood samples. An initial leukocytosis was followed by a leukopenia. The numbers of red cells, the hemoglobin concentration, and the hematocrit were increased. Nucleated red blood cells were seen in the blood smears. The serum concentration of bound calcium decreased, while phosphorus, magnesium, and potassium increased. Clinical screening tests detected no evidence of a coagulopathy in swine given T-2 toxin intravascularly.
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PMID:Experimental T-2 toxicosis in swine. II. Effect of intravascular T-2 toxin on serum enzymes and biochemistry, blood coagulation, and hematology. 406 62

Liver damage in a woman who had taken an overdose of paracetamol and dextropropoxyphene was assessed by monitoring serum prealbumin concentrations and by routine plasma enzyme determinations. The plasma aspartate aminotransferase returned to normal levels after 3 days, alkaline phosphatase was slow to show increases in activity, and serum albumin concentration was in the normal range throughout. Prothrombin-time, although initially very high, returned almost to normal as a result of the administration of plasma. In contrast, serum prealbumin concentration decreased significantly after 36 h and continued to decrease, showing the course of failing liver function, until the patient's death 15 days after presentation. Prealbumin, a functional plasma protein synthesised in the liver, has a short half-life, is a true index of liver function, and seems to be a more reliable indicator of liver function in drug overdose than plasma enzymes, prothrombin-time, or plasma drug concentration.
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PMID:Prealbumin as an index of liver function after acute paracetamol poisoning. 610 95

Sixteen clinically normal, healthy ponies were randomly assigned to 4 groups and given aflatoxin B1 in doses of 0.045, 0.030, 0.015, and 0 (control) mg/kg of body weight per day for 21 days (or total doses of 0.945, 0.630, 0.315, and 0 mg/kg). The animals were allowed to recover for 3 months and then were reassigned to 4 treatment groups such that each group during the 2nd trial included a pony from each of the groups of the 1st trial. The animals in the new groups were intubated and were given aflatoxin in doses of 0.4, 0.2, 0.1, and 0 (control) mg/kg/day for 5 days ( or total doses of 2.0, 1.0, 0.5, and 0 mg/kg). Venous blood samples were drawn every other day to monitor for toxicosis; examinations were made for RBC and WBC counts, hemoglobin concentration, PCV, serum urea nitrogen, prothrombin time, and serum concentrations of aspartate aminotransferase, iditol dehydrogenase, alkaline phosphatase, albumin, gamma-glutamyl transferase, and arginase. There were no significant differences between treatment groups and controls (given no aflatoxin) in the toxicologic values examined for during the 1st trial. During the 2nd experiment, 2 of the ponies in the large-dose treatment gorup (2.0 mg/kg) demonstrated increased serum enzyme activities. These animals had been in the large-dose (0.945 mg/kg) and median-dose (0.63 mg/kg) groups during the 1st trial. Arginase, iditol dehydrogenase, and gamma-glutamyl transpeptidase activities became increased on the 4th day of treatment and continued to increase until the 6th day of the experiment (1 day after treatment was terminated). These enzymes approached control group values at 10 days after cessation of treatment. These increases were indicative of hepatocellular toxicity. It was concluded that the possibility of equine aflatoxicosis exists although ponies given high quality rations appear to be less susceptible than some other species. Prior exposure to aflatoxins may predispose to clinical toxicity on subsequent exposure, despite lack of expression of clinical signs.
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PMID:Effects of aflatoxins in young ponies. 612 12

Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs included increased rectal temperature, faster heart and respiratory rates, abdominal straining, bloody feces, and tetanic convulsions. At necropsy, ponies that died of acute aflatoxicosis showed visceral petechiae and hepatic focal lesions. Histopathologic changes included severe hepatic necrosis, vacuolation, and bile duct hyperplasia. Aflatoxins B1 and M1 were recovered from liver, kidney, skeletal muscle, and gastrointestinal contents. One other pony given the 2 mg/kg dose died 32 days after dosing, and 1 control pony died after 70 days. Continuous elevations in prothrombin time and serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transpeptidase levels were observed in ponies dosed at 4 mg/kg or more. Significant (P less than 0.05) elevations in these values, which peaked 2 to 3 days after dosing, were seen in ponies given the 2 mg/kg dose. This group also had significant increases over controls in PCV and hemoglobin concentration 5 days after dosing.
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PMID:Acute experimentally induced aflatoxicosis in the weanling pony. 613 67

Six cases of severe leptospiral infection with renal failure are described. Five of the six patients had acute oliguric renal failure requiring dialysis. Renal function recovered over three weeks and by two months all patients had plasma creatinine levels less than 200 mumol/litre. The initial diagnosis of leptospirosis depended on clinical and epidemiological features because serological confirmation was not possible during the first week of the illness. All the patients had either high risk occupations or a history of exposure to external sources of infection. All had fever, myalgia, jaundice and muscle tenderness. Although bilirubin levels were high (greater than 350 mumol/litre in five) the elevations of aspartate transaminase and alkaline phosphatase levels, and prolongations of prothrombin times were relatively slight. Thrombocytopenia occurred in five of the six cases. Leptospira complement fixation tests were weakly positive or negative on admission in five cases but rose to significant levels subsequently. Penicillin treatment resulted in Jarisch-Herxheimer reactions in three cases. The important complications were: upper gastro-intestinal haemorrhage (five cases), thrombocytopenia less than 30 000 platelets/mm3 (four cases), atrial fibrillation (three cases), drowsiness with asterixis (four cases). All six patients were seriously ill and required intensive supportive therapy. All survived.
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PMID:Acute renal failure due to leptospirosis: clinical features and outcome in six cases. 633 67

Circulating immune complexes (CIC) were measured in 133 biopsy-proven patients with various liver diseases. The correlation between CIC levels and other laboratory findings was investigated in each disease group, in order to assess if the increased C1q-binding activity found in these patients was related to particular features of the disease. CIC levels were not significantly different in HBsAg-positive and HBsAg-negative patients. No correlation was found between CIC levels and serum bilirubin, AST, ALT and C3 levels. A negative correlation with C4 levels and a positive correlation with immunoglobulin levels were found in the majority of the patients, while prothrombin time and albumin levels were negatively correlated to CIC levels only in patients with chronic active hepatitis. Increased CIC levels could represent a response to gut-associated antigens, a passive accumulation due to reduced hepatic function or both.
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PMID:Significance of circulating C1q-binding activity in chronic liver disease: a study of 133 cases. 633 89

The characteristics of 86 patients with acute non-A, non-B hepatitis were compared to 23 patients with acute hepatitis A and 76 with acute hepatitis B by medical record reviews of patients seen at 5 hospitals in Baltimore, Maryland, as part of case-control study of viral hepatitis. Results of serum aminotransferase levels, bilirubin, albumin, and prothrombin times alone could not distinguish the type of viral hepatitis because of extensive overlap. The alanine aminotransferase range for non-A, non-B hepatitis was 56 to 1819 IU/liters, for hepatitis A 250 to 1995 IU/liters, and for hepatitis B 203 to 2120 IU/liters. The ranges of aspartate aminotransferase and bilirubin for the types of hepatitis also overlapped. Fewer patients with non-A, non-B hepatitis or hepatitis A had a prolonged prothrombin time compared to patients with hepatitis B. Hepatic encephalopathy was seen only in two patients with hepatitis B. Forty-two percent of non-A, non-B hepatitis patients followed for 6 months or longer continued to have elevated alanine aminotransferase levels. Chronic alanine aminotransferase elevation was independent of the source of infection: transfusion, parenteral drug use, or all other sources. Prolonged follow-up is necessary to evaluate chronicity in patients with non-A, non-B hepatitis.
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PMID:Community-acquired non-A, non-B hepatitis: clinical characteristics and chronicity. 642 May 13

A patient with adult polycystic liver and kidney disease presented with haematemesis and melaena and was found to have raised serum creatinine, aspartate transaminase, and alkaline phosphatase values; hypoalbuminaemia; and a prolonged prothrombin ratio. She also had oesophageal varices. With haemodialysis her aspartate transaminase activity fell to normal but she remained hypoalbuminaemic with a prolonged prothrombin ratio. She died after three weeks. Although hepatic cysts do occur in adult polycystic kidney disease, they have been thought not to cause major liver disease. The hepatic cysts in this patient, however, did appear to be associated with portal hypertension and impaired hepatocellular function.
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PMID:Bleeding oesophageal varices and hepatic dysfunction in adult polycystic kidney disease. 642 45


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