Alanine transferase

Enzymes, measured in clinical laboratories, for which kits are available include y-glutamyl transferase (GGT), alanine transferase [9000-86-6] (ALT), aldolase, a-amylase [9000-90-2] aspartate aminotransferase [9000-97-9], creatine kinase and its isoenzymes, galactose-l-phosphate uridyl transferase, Hpase, malate dehydrogenase [9001 -64-3], 5 -nucleotidase, phosphohexose isomerase, and pymvate kinase [9001-59-6]. One example is the measurement of aspartate aminotransferase, where the reaction is followed by monitoring the loss of NADH ... 

Older adults are particularly susceptible to a potentially fatal hepatitis when taking isoniazd, especially if they consume alcohol on a regular basis. Two other antitubercular drugs rifampin and pyrazinamide, can cause liver dysfunction in the older adult. Careful observation and monitoring for signs of liver impairment are necessary (eg, increased serum aspartate transaminase, increased serum alanine transferase, increased serum bilirubin, and jaundice). 

Alanine transferase (ALT) (formerly known as serum glutamic oxaloacetic transaminase SCOT)... 

Vigabatrin inhibits alanine transferase, and the resulting underestimation of enzyme activity could mask evidence of hepatic disease (SEDA-20,70). 

Proteins are not cleared by hepatic enzyme systems. Flowever, fiver size and function, spleen function, and macrophage function would be expected to account for variability in observed clearance of large therapeutic proteins. For instance, Sewell et al. (68) demonstrated that Kupffer cell function is decreased in aged rats, which is a function of age as much as it is of liver function. Standard measures of liver function such as alanine transferase may not provide relevant information and are rarely identified as a covariate even with small molecules. Flowever, patients with advanced liver disease such as cirrhosis may have reduced clearance due to poor liver function and reduced liver blood flow. 

Laboratory abnormalities of routine tests most commonly involve tests of liver function, and patients with acute Q fever may present with a clinical picture of acute hepatitis. Depending on the locale, reported elevations of aspartate aminotransferase, alanine transferase, or both, in the range of 2- to 3-fold higher than the upper limit of normal, are observed in 50% to 75% of patients, while elevation of the alkaline phosphatase is observed in 10% to 15% of patients. The total bilirubin can be expected to be elevated in 10% to 15% of patients with acute Q fever. The white blood cell count is usually normal the erythrocyte sedimentation rate is elevated in one third of patients.65 Mild anemia or thrombocytopenia may also be observed. 

Acute hepatitis mimicking iron overload syndrome was reported in a 35-year-old man who had been taking fo-ti (dose and duration unspecified). Laboratory studies included alanine transferase 2714 U/1 (normal <50 U/1), aspartate aminotransferase 1170 U/1 (normal <50 U/1), AP 137 U/1 (normal <130 U/1), total bilirubin 4.6 mg/dl (normal <1.4 mg/dl), direct bilirubin 3.0 mg/dl (normal <0.4 mg/dl), and ferritin 13,862 ng/ml (normal 8 to 282 ng/ml) and a fasting transferrin saturation of 86% (normal 20% to 60%). Analysis of the herbal supplement identified extracts from fo-ti including the anthraquinones emodin and physcion. The patient recovered after cessation of the herbal products, and liver function tests 4 months after hospitalization were normal (Laird et al. 2008). 

Hepatitis C (formerly called non-A, non-B hepatitis) Type of hepatitis distinguished by a high level of the liver enzyme alanine transferase, usually mild or inapparent infection but can be severe in compromised individuals. 

Pyridoxamine phosphate serves as a coenzyme of transaminases, e.g., lysyl oxidase (collagen biosynthesis), serine hydroxymethyl transferase (Cl-metabolism), S-aminolevulinate synthase (porphyrin biosynthesis), glycogen phosphoiylase (mobilization of glycogen), aspartate aminotransferase (transamination), alanine aminotransferase (transamination), kynureninase (biosynthesis of niacin), glutamate decarboxylase (biosynthesis of GABA), tyrosine decarboxylase (biosynthesis of tyramine), serine dehydratase ((3-elimination), cystathionine 3-synthase (metabolism of methionine), and cystathionine y-lyase (y-elimination). 

Serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, y-glutamyl transferase, and bilirubin may be elevated in patients with hepatobiliary disease. 

ALT, alanine aminotransferase AST, aspartate aminotransferase GGT, gamma-glutamyl transferase INR, international normalized ratio LDH, lactate dehydrogenase PT, prothrombin time. 

Oral dose of 1000, 2500, or 4000 mg/kg BW maintained at 22°C or minus 5°C for 10 h after dosing No deaths. Mild intoxication and elevated plasma alanine amino-transferase activity holding temperature did not affect toxicity 8... 

Hepatic Effects. Liver function tests (serum bilirubin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase) completed in 11 hexachloroethane workers were within the normal range (Selden et al. 1994). Plasma hexachloroethane levels in these workers, who wore protective equipment, were 7.3 + 6.04 pg/L at the time of the tests (Selden et al. 1993). Mild skin and mucous membrane irritation were reported in the exposed group, suggesting that exposure may have been through either the inhalation or dermal routes of exposure. 

Hepatic Effects. Liver function tests (serum bilirubin, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase) were not affected in 11 hexachloroethane-exposed workers who wore protective clothing (Selden et al. 1993). 

Liver injury is clinically defined as an increase of serum alanine amino transferase (ALT) levels of more than three times the upper limit of normal and a total bilirubin level of more than twice the upper limit of normal [4]. The clinical patterns of liver injury can be characterized as hepatocellular (with a predominant initial elevation of ALT), cholestatic (with an initial elevation of alkaline phosphatase) or mixed. The mechanisms of drug-induced hepatotoxicity include excessive generation of reactive metabolites, mitochondrial dysfunction, oxidative stress and inhibition of bile salt efflux protein [5]. Better understandings of these mechanisms in the past decades led to the development of assays and models suitable for studying such toxic mechanisms and for selecting better leads in the drug discovery stage. 

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