Prognostic Value of Serum γ-Glutamyl Transpeptidase Activity in Liver Disease

Abstract

The serum activity of γ-glutamyl transpeptidase (γ-GT) has been studied and compared with that of other serum enzymes in patients with hepatobiliary diseases. The increase of γ-GT activity in acute hepatitis begins later and lasts longer than those of the other enzymes. In mild cirrhosis with enlarged liver higher activities of serum γ-GT than in advanced atrophic cirrhosis were observed. In chronic hepatic disease a fall of serum γ-GT may indicate an unfavourable prognosis.

Enzyme assays in liver disease.

“…A number of laboratories have since reported their experience, the reports being generally favourable Kammeraat, 1970;Villa, Dioguardi, Agostoni, Ideo, and Stabilini, 1966;Lukasik, Richterich, and Colombo, 1968;Fritzsche, 1969a andZein and Discombe, 1970). Our own experience extends to more than 600 determinations.…”

γ-Glutamyl Transpeptidase: a Clinical and Experimental Study

“…This hypothesis is supported by the assay of y-GT levels in hepatic tissue of rats treated with bile duct ligation. Moreover, this is the only mechanism which is able to explain the lower y-GT elevations observed during advanced atrophic cirrhosis in respect to mild cirrhosis with enlarged liver [23][24], In this disease a significant corre lation between y-GT and cholinesterase, which is a sensitive marker of liver protein synthesis, has been observed [9], The observation that in liver cirrhosis the improvement of liver functions is paralleled by a decrease of y-GT serum levels, suggests that such decrease is not due to decreased cholestasis but to the decreased protein synthesis within the liver cells. The mechanism of y-GT increase would be similar to that of AP as it has been lately observed by Kaplan and Righetti [11].…”

Serum gamma-glutamyl transpeptidase activity in myocardial infarction.

“…Since the y-GT seems to be located in the cellular microsome fraction (Villa et al, 1965), it might be thought that it would appear later and more slowly in the series because the damage to these structures represents the last effect of the anoxic injury to the myocardial cell. If this is the case the process of liberation of enzymes from cardiac cells would be as follows (Table).…”