Protein induced by vitamin K absence or antagonist II as a prognostic marker in hepatocellular carcinoma. Comparison with alpha-fetoprotein
- PMID: 7513601
- DOI: 10.1002/1097-0142(19940515)73:10<2464::aid-cncr2820731004>3.0.co;2-9
Protein induced by vitamin K absence or antagonist II as a prognostic marker in hepatocellular carcinoma. Comparison with alpha-fetoprotein
Abstract
Background: Protein induced by vitamin K absence or antagonist II (PIVKA-II) was widely used as a diagnostic marker for hepatocellular carcinoma (HCC), however, its prognostic value is unclear. The authors evaluated PIVKA-II clinicopathologically as a prognostic marker for HCC.
Methods: The relationship between pathologic prognostic factors and plasma PIVKA-II and alpha-fetoprotein (AFP) was investigated in 72 patients with resectable HCC measuring less than 6 cm in greatest dimension.
Results: PIVKA-II shows significantly lower sensitivity, but higher specificity than AFP, and the use of these two complementary markers appears to be useful in the diagnosis of HCC. The frequencies of intrahepatic metastasis, portal vein tumor thrombus, hepatic vein tumor thrombus, and capsular infiltration were significantly higher in patients with positive PIVKA-II than in those with negative-PIVKA-II, and the recurrence-free rate was significantly lower in patients with positive rather than with negative PIVKA-II. However, there were no significant differences between the patients who were AFP positive and those who were AFP negative in pathologic prognostic factors and the recurrence-free rate. From univariate and multivariate analyses, the authors find that PIVKA-II is one of the risk factors for recurrence of HCC after hepatectomy.
Conclusions: PIVKA-II may be a useful marker for the prediction of intrahepatic spread and for the prognosis of HCC. In addition, PIVKA-II-positive patients, thus, need aggressive postoperative adjuvant therapy for undetectable residual tumors and careful postoperative monitoring to enable the early recognition of recurrence.
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