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PubMed1999

The clinical significance of slightly to moderately increased liver transaminase values in asymptomatic patients.

BACKGROUND: Our aim was to study liver disorders in asymptomatic patients with slightly to moderately increased liver transaminase values in a population living in an area with a low prevalence of viral and hereditary liver diseases. METHODS: One hundred and fifty consecutive patients with slightly to moderately increased liver transaminases for at least 6 months without symptoms or signs of liver disease were included. Median (range) was 0.75 microkat/l (0.24-2.9) for aspartate aminotransferase (ASAT) and 1.18 microkat/l (0.28-4.5) for alanine aminotransferase (ALAT). A percutaneous liver biopsy was performed, and blood was sampled for a detailed biochemical and serologic profile. RESULTS: Chronic viral hepatitis C was found in 15.3% of the patients, autoimmune hepatitis in 1.3%, primary biliary cirrhosis in 1.3%, and heterozygotic alpha-1-antitrypsin deficiency in 0.7%. Presumed alcoholic liver disease was diagnosed in 8%, and non-alcoholic steatohepatitis in 2%. Chronic hepatitis with no obvious etiology was diagnosed in 24%, of whom 39% had interface hepatitis (piecemeal activity). Seventy-one per cent of these 39% had measurable levels of autoantibodies, but IgG levels within normal limits prevented the 'clinical' diagnosis of autoimmune hepatitis. Liver steatosis was the diagnosis in 40%. Most were overweight and had increased serum triglyceride levels. However, in 13.3% the fatty infiltration was considered 'essential', as both body mass index (BMI) and triglyceride levels were normal. Other diagnoses were liver fibrosis with no obvious inflammatory activity (3.3%), cirrhosis of unknown etiology (0.7%), and for the remaining (3.3%) patients histopathologic findings were considered 'normal'. Cirrhosis was found in five biopsy specimens: hepatitis C (n = 2), autoimmune hepatitis (n = 1), primary biliary cirrhosis (n = 1), and cryptogenic cirrhosis (n = 1). No concomitant disease was of importance for the diagnosis and/or histopathologic findings. No obvious drug-related increased liver test results were found with any single drug. However, patients with chronic hepatitis of unknown etiology, especially with interface hepatitis, significantly more often than the rest of the population were receiving drug treatment. CONCLUSION: Most transaminitis patients had steatosis, and some had defined diseases including chronic hepatitis C. Chronic hepatitis of unknown etiology was found in a substantial proportion (24%) of a population living in an area with a low burden of hepatic viruses and genetic disorders.

Alanine Transaminase↗
PubMed1974

Regulation of phosphoenolpyruvate carboxykinase and tyrosine transaminase in hepatoma cell cultures. 3. Comparative studies in H35, HTC, MH1C1 and RLC cells.

The ability of N(6), O(2)'-dibutyryl cyclic AMP (DBcAMP) to regulate a number of metabolic events in four lines of cultured rat hepatomas has been examined. Although dexamethasone induces tyrosine transaminase in all four lines, DBcAMP induces this enzyme normally only in H35 cells. A slight increase in transaminase activity was seen with MH(1)C(1) cells and HTC cells, but no effect was detectable in RLC cells. In contrast, phosphoenolpyruvate carboxykinase activity is increased by both agents in H35 and MH(1)C(1) cells, but neither had any effect in HTC or RLC cells. DBcAMP caused a rapid inhibition of the growth rate and DNA synthesis and an increase in protein content in both H35 and MH(1)C(1) cells but not in HTC or RLC cells. The effect of DBcAMP on DNA synthesis in MH(1)C(1) cells could be reversed by deoxycytidine as is also the case with H35 cells. The resistance of HTC and RLC cells to DBcAMP was not due to reduced uptake or deacylation as judged by studies with [(3)H]DBcAMP. The cyclic nucleotide appears to enter the cells by passive diffusion as the intracellular concentration approaches that in the medium within 30-60 min. Possible explanations for the differential responses observed are discussed.

Animals↗
PubMed1976

Extreme elevation of transaminase levels in acute heart disease-a problem in differential diagnosis?

Five patients admitted to the Coronary Care Unit at the Department of Medicine, Serafimerlasarettet, who developed extreme elevation of transaminase levels, are discussed in terms of problems in differential diagnosis. All five had manifest right ventricular failure on admission and four also had hypotension. Three of the patients died, two survived. The three post-mortem examinations showed extensive infarctions of the left ventricle and septum. The two survivors had had a prolonged ventricular tachycardia and a probable silent infarct, respectively. It is concluded that the extremely high transaminase levels sometimes seen in acute cardiac disease are predominantly due to sizeable amounts released by the liver as a result of central necrosis of the liver cells. The probable prerequisite for the development of central necrosis of the liver in acute cardiac disease is usually the combination of right ventricular failure and hypotension, which in turn are most often due to extensive left ventricular infarcts.

Acute Disease↗
PubMed1988

Changes of serum HBV-DNA in relation to serum transaminase level during acute exacerbation in patients with chronic type B hepatitis.

To examine the relationship between changes of serum hepatitis B virus-dexoyribonucleic acid (HBV-DNA) and transaminase levels during acute exacerbation of chronic type B hepatitis, serial serum specimens from 74 patients were assayed for HBV-DNA by slot blot hybridization with 32P-labeled cloned HBV-DNA as probe. Of these patients, serial serum specimens were obtained with an interval of 2-7 days in 22 patients (Group I), 8-14 days in 30 patients (Group II) and 15-30 days in 22 patients (Group III). The peak of serum HBV-DNA was reached shortly before or simultaneously with the maximum elevation of serum alanine transaminase (ALT) in most (greater than 90%) of the acute exacerbations. In contrast, the peak of serum ALT was reached before maximum elevation of serum HBV-DNA in only 13.6% of Group I, 3.3% of Group II and 13.6% of Group III (9.5% of whole series). The results suggest that the increase of serum HBV-DNA is an event preceding, rather than the result of, hepatocytolysis in most of the acute exacerbations occurring in patients with chronic type B hepatitis.

Alanine Transaminase↗
PubMed1970

Posttranscriptional control in the steroid-mediated induction of hepatic tyrosine transaminase.

The purine analog azaguanine does not inhibit the initial induction of hepatic tyrosine transaminase by hydrocortisone. However, the continued induced synthesis of tyrosine transaminase, elicited by repeated doses of hydro-cortisone, is inhibited approximately 64 percent in the presence of the analog after 7 to 8 hours and appears to be almost completely inhibited by 9 to 10 hours; this suggests that the induction cycle involves the activation and renewal of a pool of preexisting messenger RNA.

Adrenalectomy↗
PubMed1970

Tyrosine transaminase induction by dexamethasone in a new rat liver cell line.

A cell line derived from normal, adult rat liver has been established; the cells are similar to hepatocytes, as shown by electron microscopy. The addition of dexamethasone to the culture medium induced a three- to sixfold increase in the specific activity of tyrosine alpha-ketoglutarate transaminase; this increase was inhibited by the simultaneous addition of cycloheximide or actinomycin D. The latter, when added to cells given prior treatment with dexamethasone, further enhanced the transaminase activity. Contact-inhibited cells showed a lower response to dexamethasone than exponentially growing cells.

Animals↗
PubMed1971

Inhibition of growth of Salmonella typhimurium and of threonine deaminase and transaminase B by beta-chloroalanine.

beta-Chloro-l-alanine (CA) was found to inhibit the growth of Salmonella typhimurium. The inhibition was overcome by isoleucine plus valine. CA inhibited the activity of threonine deaminase and transaminase B in vitro. The inhibition of threonine deaminase was reversible and was not affected by desensitization to isoleucine inhibition. Transaminase B was irreversibly inactivated. Derepression of some of the isoleucine and valine biosynthetic enzymes was achieved by growth of wild-type cells on low levels of CA.

Alanine↗
PubMed1987

Cloning and characterization of the Escherichia coli K-12 alanine-valine transaminase (avtA) gene.

avtA, which encodes the alanine-valine transaminase, transaminase C, was cloned in vivo with high- and low-copy-number mini-Mu cloning vectors. The phenotype conferred by the cloned avtA+ gene usually depended upon the plasmid copy number; most high-copy-number avtA+ plasmids permitted isoleucine-requiring ilvE strains to grow in the absence of isoleucine (multicopy suppression), while low-copy-number avtA+ plasmids did not. avtA was mapped to a 1.25-kilobase segment by comparison of the restriction maps of 24 independent mini-Mu plasmids and then by gamma-delta (Tn1000) mutagenesis of a pBR322-avtA+ plasmid. The direction of transcription of avtA on the cloned fragment was determined with fusions to a promoterless lac gene.

Chromosome Mapping↗
PubMed1991

A functional leuABCD operon is required for leucine synthesis by the tyrosine-repressible transaminase in Escherichia coli K-12.

In Escherichia coli K-12, two enzymes, encoded by ilvE and tyrB, catalyze the amination of 2-ketoisocaproate (2-KIC) to form leucine. Although leucine-requiring derivatives of an ilvE strain that are unable to grow on 2-KIC were expected to have mutations only in tyrB, mapping studies showed that one such mutation was tightly linked to the leu operon (at 1.5 min), not to tyrB (at 92 min). Chromosomal fragments cloned because they complemented this mutation were found to complement leu mutations, and vice versa, but none of these fragments complemented a tyrB mutation. The Tn5 insertion and flanking host DNA from this anomalous mutant was cloned in vivo, using Mu dII4042, and an in vivo procedure was developed to isolate deletion derivatives of Tn5-containing plasmids. These deletion plasmids were used to determine the DNA sequences flanking the transposon. The data showed that Tn5 was inserted between bp 122 and 132 in the leu leader. In addition, other ilvE leu double mutants were found to be unable to grow on 2-KIC in place of leucine. The accumulation of 2-ketoisovalerate in ilvE leu double mutants was shown to interfere with 2-KIC amination by the tyrB-encoded transaminase and also by the aspC- and avtA-encoded transaminases (which are able to catalyze this reaction in vivo when the corresponding genes are present on multicopy plasmids).

Bacteriophages↗
PubMed1999

Synergistic operation of the CAR2 (Ornithine transaminase) promoter elements in Saccharomyces cerevisiae.

Dal82p binds to the UIS(ALL) sites of allophanate-induced genes of the allantoin-degradative pathway and functions synergistically with the GATA family Gln3p and Gat1p transcriptional activators that are responsible for nitrogen catabolite repression-sensitive gene expression. CAR2, which encodes the arginine-degradative enzyme ornithine transaminase, is not nitrogen catabolite repression sensitive, but its expression can be modestly induced by the allantoin pathway inducer. The dominant activators of CAR2 transcription have been thought to be the ArgR and Mcm1 factors, which mediate arginine-dependent induction. These observations prompted us to investigate the structure of the CAR2 promoter with the objectives of determining whether other transcription factors were required for CAR2 expression and, if so, of ascertaining their relative contributions to CAR2's expression and control. We show that Rap1p binds upstream of CAR2 and plays a central role in its induced expression irrespective of whether the inducer is arginine or the allantoin pathway inducer analogue oxalurate (OXLU). Our data also explain the early report that ornithine transaminase production is induced when cells are grown with urea. OXLU induction derives from the Dal82p binding site, which is immediately downstream of the Rap1p site, and Dal82p functions synergistically with Rap1p. This synergism is unlike all other known instances of Dal82p synergism, namely, that with the GATA family transcription activators Gln3p and Gat1p, which occurs only in the presence of an inducer. The observations reported suggest that CAR2 gene expression results from strong constitutive transcriptional activation mediated by Rap1p and Dal82p being balanced by the down regulation of an equally strong transcriptional repressor, Ume6p. This balance is then tipped in the direction of expression by the presence of the inducer. The formal structure of the CAR2 promoter and its operation closely follow the model proposed for CAR1.

5' Untranslated Regions↗
PubMed2004

Reduced transaminase B (IlvE) activity caused by the lack of yjgF is dependent on the status of threonine deaminase (IlvA) in Salmonella enterica serovar Typhimurium.

The YjgF/YER057c/UK114 family is a highly conserved class of proteins that is represented in the three domains of life. Thus far, a biochemical function demonstrated for these proteins in vivo or in vitro has yet to be defined. In several organisms, strains lacking a YjgF homolog have a defect in branched-chain amino acid biosynthesis. This study probes the connection between yjgF and isoleucine biosynthesis in Salmonella enterica. In strains lacking yjgF the specific activity of transaminase B, catalyzing the last step in the synthesis of isoleucine, was reduced. In the absence of yjgF, transaminase B activity could be restored by inhibiting threonine deaminase, the first enzymatic step in isoleucine biosynthesis. Strains lacking yjgF showed an increased sensitivity to sulfometruron methyl, a potent inhibitor of acetolactate synthase. Based on work described here and structural reports in the literature, we suggest a working model in which YjgF has a role in protecting the cell from toxic effects of imbalanced ketoacid pools.

Bacterial Proteins↗
PubMed1960

Serum transaminases and isocitric dehydrogenase in kwashiorkor.

Serum glutamic oxalacetic transaminase (G-OT), glutamic-pyruvic transaminase (G-PT), and isocitric dehydrogenase (ICD) have been estimated in six groups of subjects, namely, normal British adults, normal Nigerian adults, undernourished Nigerian adults and children, Nigerian children with florid protein malnutrition (kwashiorkor), and cases of protein malnutrition after treatment. The normal range in Nigerian adults was apparently slightly lower than in European adults.A marked increase in serum enzyme activity was found in florid malnutrition, and a slight rise in undernutrition. In all cases serum G-PT showed lesser changes than G-OT and ICD. The causes of these abnormalities are discussed. The increased serum enzyme activity is thought to be derived primarily from the liver and possibly also from voluntary muscle. Estimation of serum enzymes is recommended in the investigation of protein malnutrition.

Humans↗
PubMed1977

Purification and partial characterization of cysteine-glutamate transaminase from rat liver.

Cysteine-glutamate transaminase (cysteine aminotransferase; EC 2.6.1.3) has been purified 149-fold to an apparent homogeneity giving a specific activity of 2.09 IU per milligram of protein with an overall yield of 15%. The isolation procedures involve the preliminary separation of a crude rat liver homogenate which was submitted sequentially to ammonium sulfate fractionation, TEAE-cellulose column chromatography, ultrafiltration, and isoelectrofocusing. The final product was homogenous when examined by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate (SDS). A minimal molecular weight of 83 500 was determined by Sephadex gel chromatography. The molecular weight as estimated by polyacrylamide gel electrophoresis in the presence of SDS was 84 000. The purified enzyme exhibited a pH optimum at 8.2 with cysteine and alpha-ketoglutarate as substrates. The enzyme is inactivated slowly when kept frozen and is completely inactivated if left at room temperature for 1 h. The enzyme does not catalyze the transamination of alpha-methyl-DL-cysteine, which, when present to a final concentration of 10 mM, exhibits a 23.2% inhibition of transamination of 30 mM of cysteine. The mechanism apparently resembles that of aspartate-glutamate transaminase (EC 2.6.1.1) in which the presence of a labile hydrogen on the alpha-carbon in the substrate is one of the strict requirements.

Amino Acids↗
PubMed1982

Increased serum bile acids in cirrhosis with normal transaminases.

Fasting and postprandial serum concentrations of total conjugated primary bile acids determined by radioimmunoassay have been compared with conventional liver function tests in patients with cirrhosis of the liver and normal transaminases. While gamma-glutamyl-transferase had the highest sensitivity (69%) among the conventional liver function tests, it was much less sensitive for the detection of cirrhosis with normal transaminases than fasting (93% sensitivity) or postprandial (93% sensitivity) bile acid concentrations in serum. When a combination of fasting and postprandial bile acid concentrations was used, the sensitivity increased to 97%.

Adult↗
PubMed1990

Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor.

The GABA-transaminase inhibitor, vigabatrin, has been shown to have a rather low degree of acute toxicity in several animal species. Oral administration of the drug at 1,000 mg/kg/day for 2-4 weeks caused decreased food consumption and weight loss with resultant prostration and death in both rats and dogs. Dosages of 200 mg/kg/day were tolerated for a year without clinical signs in dogs, although rats suffered reduced weight gains and convulsions after 3-4 months when given the drug in the diet. The convulsions continued to occur frequently throughout the one-yr study, but abated 3-4 months after cessation of treatment. The only consistent histopathologic evidence of toxicity in rats and dogs has been the finding of intramyelinic edema (microvacuolation) in the brain, most notably in certain areas of white matter (cerebellum, reticular formation and optic tract in rats and columns of fornix and optic tract in dogs). No lesions were found in the spinal cord or peripheral nervous system. It took several weeks for the microvacuolation to develop, even at high dosages, but it did not continue to progress thereafter, even though a slight effect was noted at dosages as low as 30-50 mg/kg/day after one yr of treatment. The intramyelinic edemia disappeared within a few weeks after treatment was withdrawn. No residual effects were observed in dogs, whereas rats exhibited swollen axons and microscopic mineralized bodies in the cerebellum. Monkeys exhibited no adverse clinical effects except for occasional loose stools at 300 mg/kg/day. After 16 months of oral treatment at 300 mg/kg/day any suggestion of intramyelinic edema was considered to be equivocal, and there was no evidence of any effect in the 50 or 100 mg/kg/day monkeys after 6 yr of treatment. Higher doses caused chronic diarrhea, thus limiting the dosage in this species. Vigabatrin was shown to be well absorbed in rat, dog and man, whereas dose-limited absorption occurred in the monkey. Metabolism is practically nil in all 4 species and the primary elimination pathway is by glomerular filtration. Because vigabatrin is an irreversible inhibitor of GABA-transaminase and the enzyme has a slow turnover rate, plasma levels of the drug are not indicative of its pharmacologic activity. For this reason cerebrospinal fluid levels of GABA and vigabatrin were evaluated, with considerable species differences being noted. The significance of these differences in relation to the differences in toxic response is discussed.

4-Aminobutyrate Transaminase↗
PubMed2006

Incidental raised transaminases: a clue to muscle disease.

Twenty-one patients with incidental hypertransaminasaemia who were eventually diagnosed as muscular dystrophy are described. There were two females and 19 males aged between 2 and 11 years [mean (SD) 6.7 (3.4) y]. Serum alanine and aspartate transaminase levels were between 73 and 595 IU/L (30-35) and 68 and 550 IU/L (30-35), respectively. Muscle disease was suspected when creatine phosphokinase levels were elevated and confirmed in each patient by muscle biopsy. The time interval between incidental hypertransaminasemia and the diagnosis of muscle disease was between 3 and 12 months. Eleven patients were diagnosed as Becker's muscle dystrophy, eight as Duchenne muscle dystrophy and two had sarcoglycanopathy. Long-term elevation of transaminase levels might be a sign of occult muscle disease. Invasive tests such as liver biopsy should not be performed in patients with unexplained hypertransaminasaemia without first determining creatinine phosphokinase levels.

Biomarkers↗
PubMed2005

Relationship between leptin, insulin, body composition and liver steatosis in non-diabetic moderate drinkers with normal transaminase levels.

OBJECTIVE: Obesity and insulin resistance play a major role in the development of liver steatosis (LS), but also relative leptin resistance has been reported to correlate with LS in humans. Our objective was to investigate the relationship between serum leptin, insulin, obesity and LS in non-diabetic males (n = 74) and postmenopausal females (n = 50) with normal transaminase levels and low-to-moderate alcohol intake. METHODS: A medical history to retrieve information about health status, current medications, alcohol consumption and history of viral or toxic hepatitis; a physical examination including height, weight, waist circumference and blood pressure; a fasting blood draw for the determination of glucose, insulin, leptin, lipid profile, transaminases and uric acid; an oral glucose tolerance test to exclude type 2 diabetes; a dual-energy X-ray absorptiometry scan to assess fat mass (FM) and lean body mass (LBM), and an echography of the liver to assess LS. RESULTS: Fasting leptin and insulin were highly correlated with FM in men (R = 0.767 and R = 0.495 respectively, P < 0.001) and women (R = 0.713 and R = 0.526 respectively, P < 0.001). After correction for FM, leptin showed a significant negative correlation with LBM in men (R = -0.240, P = 0.039), but not in women (R = -0.214, P = 0.132). The positive relationship observed between leptin, insulin and LS persisted after adjustment of leptin and insulin for body composition only in men (R = 0.415, P < 0.001 and R = 0.339, P = 0.003 respectively for leptin and insulin vs LS). Adjusted means (95% confidence intervals) of leptin increased significantly across categories of LS in men even when insulin was considered in the model (absent = 7.1 ng/ml (5.6-8.5), mild = 8.2 ng/ml (7.2-9.2), moderate/severe = 12.1 ng/ml (10.3-14.0); P < 0.001), whereas no significant relationship was observed between insulin and LS after leptin was accounted for. CONCLUSION: Serum concentrations of leptin and insulin are positively correlated in men independently of body composition, but not in postmenopausal women. In men, the steatogenic effect of hyperinsulinemia/insulin resistance in the context of low-to-moderate alcohol consumption appears to be mediated by high concentrations of serum leptin, whereas body fat alone could identify postmenopausal women at high risk for LS.

Aged↗
PubMed2001

Elevation of hepatic transaminases after enoxaparin use: case report and review of unfractionated and low-molecular-weight heparin-induced hepatotoxicity.

Enoxaparin, a low-molecular-weight heparin (LMWH), is widely used for the treatment and prophylaxis of thromboembolic disorders, such as deep vein thrombosis. Low-molecular-weight heparin products have smaller and more uniform molecular weights than unfractionated heparin, allowing them to exhibit a much greater affinity for factor Xa than factor IIa. Compared with traditional unfractionated heparin, LMWHs have proved to be equally efficacious and may be safer. The distinctive characteristics of LMWHs have resulted in decreased rates of bleeding and equivalent rates of thrombocytopenia compared with unfractionated heparin. This favorable safety profile has been identified in several studies and may have led clinicians to believe that LMWHs have lower frequencies of all common side effects. A 66-year-old woman developed increased hepatic transaminases during treatment with enoxaparin for a deep vein thrombosis; they returned to normal after enoxaparin discontinuation. A causal relationship between unfractionated heparin and asymptomatic, transient increases in hepatic transaminase levels has been documented; these increased levels also appear to be an underrecognized, adverse effect of LMWH therapy.

Aged↗