[Show abstract][Hide abstract]ABSTRACT: Aims/background:
This study was undertaken in order to characterize the liver injury induced by transcatheter arterial chemoembolization therapy (TACE) for hepatocellular carcinoma (HCC) and to elucidate-mechanisms involved in the growth of mononuclear phagocytes in injured human liver in vivo.
Patients and methods:
The serum levels of macrophage-colony stimulating factor (M-CSF) along with clinical parameters were examined in 43 patients with HCC who underwent TACE. Ten patients who underwent angiography alone served as controls.
Serum M-CSF increased and peaked on the third day after TACE showing significant correlations (p < 0.001, respectively) with the increases in serum alanine aminotransferase (ALT) and type IV collagen-7S (IVcol-7S). The lipopolysaccharide-stimulated production of interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha in peripheral whole blood increased and peaked on the first or on the third day after TACE. In effective cases of TACE, significantly (p < 0.05) greater increases in serum M-CSF were noted as compared with those in ineffective cases.
The serum levels of M-CSF increased after TACE in correlation with hepatic inflammation and necrosis and increased production of IL-1 beta, TNF-alpha and IL-6 in peripheral whole blood. These results suggest a mechanism by which hepatic injury enhances the production of M-CSF via a cytokine cascade, which results in the proliferation of liver macrophages in vivo.