Hepatic damage induced by transcatheter arterial chemoembolization elevates serum concentrations of macrophage‐colony stimulating factor

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. Results: 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)-1β, IL-6, and tumor necrosis factor (TNF)-α 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. Discussion: The serum levels of M-CSF increased after TACE in correlation with hepatic inflammation and necrosis and increased production of IL-1β, TNF-α, 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.