The effects of alcohol in the elevation of serum PIVKA-II level in patients without hepatocellular carcinoma

초록

Background: PIVKA-II is widely used as a specific marker for screening hepatocellular carcinoma (HCC) in patients with chronic liver disease. However we often face with the situation that the level of serum PIVKA-II is significantly elevated in patients without evidence of HCC. We aimed to evaluate the effects of alcohol in the elevation of serum PIVKA-II in the absence of HCC. Methods: People who visited Korea University Guro Hospital and checked serum PIVKA-II level during January, 2005 and March, 2012 were included and their medical records were retrospectively reviewed. There were 90 subjects whose serum PIVKA-II level were elevated equal or more than 125 mAU/mL in the absence of HCC (Group 1) during their follow-up. We determined another 90 subjects as age, sex matched control group (Group 2) who had low levels of serum PIVKA-II (< 125 mAU/mL) and no evidence of HCC. Among Group 1, 10 of the administration of vitamin K antagonist was excluded. In this study, heavy alcohol consumer was defined as taking ethanol more than 70 g/day in men and 30 g/day in women for more than 10 years. P-values <0.05 were considered statistically significant. Results: Male accounted for 73.5% and the mean age was 55.04 years. Baseline characteristics were not different between the groups except the rates of patients with liver cirrhosis (70.0% in Group 1 and 41.1% in Group 2, p-value=0.000), the rates of patients with viral-related liver disease (51.3% in Group 1 and 74.4% in Group 2, p-value=0.002). Rates of subjects who had a history of heavy alcohol consumption were significantly higher in Group 1(62.5%) than in Group 2 (20.0%) (p-value = 0.000). In univariate analysis, severity of liver cirrhosis graded by Child-Pugh class (p-value = 0.000 in CP class B and p-value = 0.001 in CP class C), an absence of viral-related liver disease (p-value =0.002) and a history of heavy alcohol consumption (p-value =0.000) were significant factors which can affect the elevation of serum PIVKA-II level. Among them, only a history of heavy alcohol consumption (OR 4.722, 95% C.I 2.101-10.613, p-value=0.000) and severity of liver cirrhosis (OR 3.107, 95%C.I 1.131-8.535, p-value=0.028 in Child-Pugh class B and OR 9.008, 95% C.I 1.712-47.391, p-value=0.009 in Child-Pugh class C) were significant by multivariate analysis. Conclusions: A history of heavy alcohol consumption and liver cirrhosis clearly affected the serum PIVKA-II level. Our study indicates that serum PIVKA-II level may not be a useful marker for detecting HCC in a patient with a history of chronic alcohol consumption or with moderate to severe liver cirrhosis.