Serum Aspartate Aminotransferase to Alanine
Aminotransferase Ratio in Human and Experimental Alcoholic
Liver Disease: Relationship to Histologic Changes

Aa, Nanji; Sw, French; Cl, Mendenhall

doi:10.1159/000469062

Cited by 12 publications

(8 citation statements)

References 7 publications

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“…The toxicity of the chelators in hepatocytes in culture was assessed from cellular morphology and from the release of the cytoplasmic enzyme AST (EC 2.6.1.1) into the overlaying medium within the time period of the uptake or mobilization experiment. The release of AST has generally been regarded as a reliable indicator for assessing the severity of cell injury (50)(51)(52). Enzyme levels were measured in aliquots of the medium (after centrifugation to remove any cellular debris) and in the cell suspension (after sonication) and expressed as a percentage of the control after correction for variation in DNA between plates.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of the iron chelation potential of hydrazones of pyridoxal, salicylaldehyde and 2-hydroxy-1-naphthylaldehyde using the hepatocyte in culture

et al. 1992

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A range of new analogues of the promising iron chelator pyridoxal isonicotinoyl hydrazone was prepared and assessed for activity in reducing hepatocyte iron, mechanism of action and potential in iron-chelation therapy. A total of 45 compounds were synthesized by condensation of aromatic aldehydes (pyridoxal, salicylaldehyde and 2-hydroxy-1-naphthylaldehyde) with various acid hydrazides prepared by systematic substitutions on the benzene ring or by the replacement of the ring with an acetyl, pyridyl, furoyl or thiophene moiety. The effects of these compounds on 59Fe uptake and intracellular distribution in hepatocytes in culture and on 59Fe mobilization from prelabeled hepatocytes were assessed. Toxicity, lipophilicity and the ability to chelate plasma transferrin-bound 59Fe were also evaluated. Several compounds were much more active than pyridoxal isonicotinoyl hydrazone and may have clinical potential. These included pyridoxal benzoyl hydrazone, pyridoxal p-methoxybenzoyl hydrazone, pyridoxal m-fluorobenzoyl hydrazone and pyridoxal 2-pyridyl hydrazone. All were more effective at reducing iron uptake than mobilizing hepatocyte iron; they also may act primarily on the transit iron pool rather than on storage iron. Other compounds (e.g., salicylaldehyde p-t-butyl-benzoyl hydrazone) redistributed ferritin-59Fe to different intracellular sites but had little net effect on hepatocyte iron levels.

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Section: Methodsmentioning

confidence: 99%

Evaluation of the iron chelation potential of hydrazones of pyridoxal, salicylaldehyde and 2-hydroxy-1-naphthylaldehyde using the hepatocyte in culture

et al. 1992

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“…Levels of AST more than 500 IU/L or an alanine aminotransferase (ALT) > 200 IU/L are uncommonly seen with alcoholic hepatitis (other than alcoholic foamy degeneration, or concomitant acetaminophen overdose),122 and should suggest another etiology. In about 70% of patients, the AST/ALT ratio is higher than 2, but this may be of greater value in patients without cirrhosis 123–125. Ratios greater than 3 are highly suggestive of ALD 126…”

Section: Diagnosismentioning

confidence: 99%

Alcoholic Liver Disease

2010

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“…The serum AST is commonly 2-6 times the upper limit of normal. Further, in 70% of patients the AST/ALT ratio is usually greater than 2; ratios greater than 3 are even more suggestive of AH (10,(32)(33)(34).…”

Section: Laboratory Findingsmentioning

confidence: 99%