Liver function in acute viral hepatitis as determined by a hepatocyte‐specific ligand: 99m Tc‐galactosyl–neoglycoalbumin

Twelve patients with recently diagnosed acute viral hepatitis underwent serial 99m Tc‐galactosyl neoglycoalbumin scanning of the liver (for up to 8 mo). Injection of 99m Tc‐galactosyl neoglycoalbumin (150 mBq) at a rate of 3.5 mg (50 nmol; 1 ml) revealed that the liver is the exclusive site of tracer uptake. Simulation of 99m Tc‐galactosyl neoglycoalbumin kinetics allowed quantification of galactosyl neoglycoalbumin binding to human hepatic binding protein. Return of liver function test scores to normal values was associated in two patients with hepatitis A, in four patients with hepatitis B and in two patients with non‐A, non‐B hepatitis virus infection, with increases in hepatic binding protein concentration (up to three times the initial concentration), binding rate constant and hepatic blood flow. In the other four patients (three patients with hepatitis B and one patient with cytomegalovirus infection) a prolonged course of disease was monitored. In the mean, hepatic binding protein increased from 0.41 ± 0.11 μmol/L after onset of acute hepatitis (n = 12) to 0.78 ± 0.21 μmol/L after 6 mo of follow‐up (n = 10) (p < 0.001). During this period, binding rate constant (72.4 ± 12.6 vs. 82 ± 11.5 μmol/L/sec; p < 0.05) and hepatic blood flow (0.027 ± 0.0051 vs. 0.031 ± 0.0083 L/sec; p < 0.05) increased. Hepatic binding protein concentration correlated highly with actual laboratory test results for liver function (r = 0.98; p = 0.0001). We conclude that scintigraphic evaluation of functional liver cell mass using the new receptor‐tracer 99m Tc‐galactosyl neoglycoalbumin could provide an in vivo diagnostic means of quantifying liver function and assessing liver morphology. In addition, our findings suggest that changes in hepatic binding protein–receptor concentration are likely to occur in vivo. (Hepatology 1992;15:593–598).