慢性肝病變患者血清中類胰島素生長因子-1、類胰島素生長因子結合蛋白-3與生長激素之檢測及其可能臨床應用研究

BACKGROUND The insulin-like growth factor system (IGFs) plays an important role in cell growth and differentiation. Nevertheless, the roles played by insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3) and human growth hormone (HGH) in the progression of chronic liver disease remain to be elucidated and investigated. METHODS The subjects in the present study included 60 healthy controls, 57 liver cirrhosis patients and 32 untreated hepatocellular carcinoma patients. Blood was drawn by venipuncture into Venoject tubes. To find the possible correlations between liver damage and IGFs, serum IGF-1, GH, IGFBP-3 concentration and related biochemical parameters were measured. We used immunoradiometric assay to determine the levels of IGF-1, HGH and IGFBP-3 in serum. RESULTS Significant higher levels of serum AST, ALT, prothrobin time and T. bilirubin in patients with liver cirrhosis and untreated hepatocellular carcinoma compared to the healthy control normal group were observed; on the contrary, the levels of serum albumin, IGF-1 and IGFBP-3 were significant lower in patients with liver cirrhosis and untreated hepatocellular carcinoma compared to the healthy control group. According to the Child-Pugh classification, we compared the difference among the patients with liver cirrhosis and found both serum IGF-1 and IGFBP-3 decresed significantly when the extent of liver cirrhosis increased; however, the HGH levels elevated when the extent of liver cirrhosis increased. The effects of alpha-fetoprotein (AFP) level on the parameters measured indicated that the IGF-1 level and IGF-1/ IGFBP-3 ratio in liver cirrhosis group were decreased significantly; on the contrary, serum AST and ALT were markedly elevated. In addition, the serum IGF-1 and IGFBP-3 levels in patients with untreated hepatocellular carcinoma were elevated significantly based on the difference in AFP level. CONCLUSION Serum IGFBP-3 may be used as a marker for the hepatic synthetic capacity and chronic liver disease development into the hepatocellular carcinoma.