Abstract
99mTc-galactosylated neoglycoalbumin (99mTc-NGA) is a hepatocyte-specific tracer that, after injection into the blood stream, delivers radioactivity selectively to the liver. This is based upon chemical recognition and binding by the hepatic binding protein (HBP), a receptor specific for galactosylated glycoproteins. Liver tissue samples were obtained intraoperatively from patients undergoing surgery for various cancers. The concentration of specific HBP receptors in the liver (normal liver, hepatoma, liver metastasis) was calculated from the in vitro binding of 99mTc-NGA. One week after surgery, the in vivo HBP density was also measured in some of these patients after injection of 3.5 mg (50 nmol per patient) 99mTc-NGA (150-200 MBq) for simulation of 99mTc-NGA kinetics. Comparison of in vitro and in vivo HBP concentration in the liver showed values in the same concentration range. In patients with hepatoma or liver metastasis a significantly (P less than 0.01) decreased global HBP density was found in vivo compared to controls. The values obtained for in vivo HBP concentration in the liver amounted to 0.38 +/- 0.05 mumol l-1 liver for patients with hepatoma, to 0.4 +/- 0.1 mumol l-1 in patients with liver metastasis and to 94 +/- 0.05 mumol l-1 liver in cancer patients without liver malignancy. In vitro investigation of HBP density revealed the malignant liver tissue to have a significantly (P less than 0.0001) decreased or almost (completely) absent HBP receptor density compared to the normal tissue apart from the cancer area. It is concluded that determination of HBP density in vivo via a specific tracer is a new, simple and reliable approach for the determination of remaining hepatic function in patients with primary or secondary liver cancer.
Highlights
0.4 ± 0.1 gAmol 1- in patients with liver metastasis and to 94 ± 0.05 timol 1- liver in cancer patients without liver malignancy
Direct evidence for reduction of hepatic binding protein (HBP) concentration as a consequence of hepatocellular pathology was obtained in studies with chemical carcinogens (Stockert & Becker, 1980), and positive correlation of reduced in vitro HBP binding activity and increased circulating inhibitors resulted from a study of galactosamine-induced liver disease (Sawamura et al, 1981)
This study investigated the in vivo binding of 99mTc-NGA to HBP in patients with normal livers, hepatomas and liver metastasis
Summary
0.4 ± 0.1 gAmol 1- in patients with liver metastasis and to 94 ± 0.05 timol 1- liver in cancer patients without liver malignancy. Stadalnik and co-workers (Stadalnik et al, 1985; Vera et al, 1985a) introduced a model for in vivo binding and simulation of a hepatocyte specific tracer, 99mTc-neoglycoalbumin C9mTc-NGA), to human hepatic binding protein (HBP; Stockert & Morell, 1983) in patients with liver disease in order to evaluate hepatic function from global HBP receptor density and hepatic blood flow. Direct evidence for reduction of HBP concentration as a consequence of hepatocellular pathology was obtained in studies with chemical carcinogens (Stockert & Becker, 1980), and positive correlation of reduced in vitro HBP binding activity and increased circulating inhibitors resulted from a study of galactosamine-induced liver disease (Sawamura et al, 1981) Based on these observations we addressed the question of whether the in vivo HBP density measured by 9'Tc-NGA scintigraphy would be changed in patients with primary or secondary liver cancer. This was assessed in liver tissue samples (normal liver, hepatoma, liver metastasis)
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