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A Study of Transaminase and Alkaline Phosphatase Levels in Normal Persons and Those with Gallbladder Disease

SANFORD M. MOSSBERG, M.D.; ALAN BLOOM, M.D.; JESSE BERKOWITZ, M.D.; GEORGE ROSS, B.S.

Arch Intern Med. 1962;109(4):429-437.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 necrosis^10-14 and a host of other disease states^5,6,15-21 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 . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Division of Medicine and the Laboratory Division, Montefiore Hospital.

Footnotes
Submitted for publication Jan. 14, 1961.

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