@Article{Adamek2012,
journal="Contemporary Oncology/Współczesna Onkologia",
issn="1428-2526",
volume="16",
number="3",
year="2012",
title="Alterations of insulin-like growth factor I (IGF-I) and estradiol serum  	levels in chronic hepatitis C",
abstract=" Aim of the study:  Deregulation of insulin-like growth factor I (IGF-I) production and decreased hepatic estrogen levels were associated with development of hepatocellular carcinoma (HCC) in hepatitis C virus (HCV) infected cirrhotic patients. The aim of our study was to determine serum levels of IGF-I, insulin and 17-β estradiol (17-βE) in relation to other markers of liver injury in chronic hepatitis C (CHC) patients.   Material and methods : Thirty anti-viral treatment-naïve CHC patients and 10 healthy subjects were examined. HCV infection was confirmed by presence of anti-HCV and HCV-RNA in serum. Serum levels of IGF-I, insulin and of 17-βE were evaluated using ELISA methods.   Results : Serum levels of IGF-I and 17-βE were significantly lower in CHC patients than in controls while insulin levels were similar in both groups. A lower   IGF-I level (but not the level of 17-βE)   was observed in cirrhotic CHC patients in comparison to non-cirrhotic ones. Decreased serum level of IGF-I was associated with more advanced staging and liver steatosis, higher levels of alpha-fetoprotein (AFP) and gamma globulin levels, and higher aspartate transaminase (AST) activity in CHC patients. Insulin and 17-βE levels positively correlated with patient’s age. A positive correlation was observed between insulin level on one hand and staging, liver steatosis and levels of gamma globulins in CHC patients on the other. A negative correlation between IGF-I and insulin levels was noted only in HCV infected patients.   Conclusions : Decreased IGF-I levels and increased levels of insulin better than estradiol serum levels characterize staging and liver steatosis in CHC patients. The lower serum level of 17-βE in the CHC group than in control patients suggests that CHC patients carry higher risk of liver injury and of HCC development.",
author="Adamek, Agnieszka
and Kasprzak, Aldona
and Seraszek, Agnieszka
and Mikoś, Hanna
and Bura, Aleksandra
and Mozer-Lisewska, Iwona",
pages="234--239",
doi="10.5114/wo.2012.29291",
url="http://dx.doi.org/10.5114/wo.2012.29291"
}