An increase of serum glutamic oxalacetic transaminase (SGO-T) activity following myocardial infarction was first described by LaDue et al.1 and subsequently confirmed by numerous investigators.2-6 Much emphasis has been placed on elevated SGO-T values in substantiating the clinical impression of myocardial infarction, especially when the electrocardiogram reveals equivocal changes, previous infarction, left bundle branch block, or arrhythmia.7-9 With increased understanding of the ubiquitous nature of GO-T distribution in human tissues, it has become apparent that liver necrosis10-14 and a host of other disease states5,6,15-21 can provoke a rise in SGO-T activity. Thus, confusion may still exist when there is elevated SGO-T activity in the absence of electrocardiographic evidence of heart muscle damage.
Obstructive biliary tract disease causes a rise in SGO-T activity,22,23 and this rise may be unrelated to hepatic necrosis.24 The demonstration of high GO-T activity in bile25 further serves to
MOSSBERG SM, BLOOM A, BERKOWITZ J, ROSS G. Serum Enzyme Activities Following MorphineA Study of Transaminase and Alkaline Phosphatase Levels in Normal Persons and Those with Gallbladder Disease. Arch Intern Med. 1962;109(4):429–437. doi:10.1001/archinte.1962.03620160055008
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