Abstract
Association between variable agent-induced hepatocellular carcinoma (HCC) and both
PAI-1
4G/5G polymorphism and plasminogen activator inhibitor (PAI-1) levels compared to healthy controls have been reported in earlier studies. We aimed to assess serum PAI-1 and
PAI-1
4G/5G polymorphism in hepatitis C virus (HCV)-induced HCC, HCV-induced liver cirrhosis, and viral infection-free apparently healthy control subjects. Forty nine HCC, 52 cirrhosis, and 105 controls were genotyped for
PAI-1
4G/5G using an allele-specific polymerase chain reaction analysis. In addition, for 31 HCC, 24 cirrhosis, and 28 controls, serum PAI-1 level was measured by enzyme-linked immunosorbent assay (ELISA). There was no significant difference in
PAI-1
4G/5G genotype distribution between cirrhosis and controls (
p
= 0.33,
p
= 0.15, and
p
= 0.38 for the codominant, dominant, and recessive models, respectively) or between HCC and cirrhosis (
p
= 0.5,
p
= 0.24, and
p
= 0.69 for the codominant, dominant, and recessive models, respectively). Serum PAI-1 was significantly higher in cirrhosis than controls and significantly lower in HCC than cirrhosis (
p
< 0.001 for both). Serum PAI-1 did not differ significantly among the three
PAI-1
4G/5G genotypes in controls, cirrhosis, and HCC (
p
= 0.29,
p
= 0.28, and
p
= 0.73 respectively). We documented higher serum PAI-1 in HCV-induced HCC than viral infection-free controls, but interestingly, lower than HCV-induced liver cirrhosis patients. This was not genotype related. Further studies will be needed to clearly elucidate the underlying mechanism.