Abstract

AimTo evaluate the correlation of serum PIVKA-II levels and development of portal vein tumor thrombus (PVTT) in hepatocellular carcinoma (HCC) patients.MethodsOne hundred and twenty-three patients with newly diagnosed HCC were included in this study between March 2016 and October 2018. Thirty-five of these patients were detected with PVTT and all subjects were randomly divided to analysis group (N = 73) and validation (N = 50) group. Serum levels of PIVKA-II, laboratory tests including serum aspartate aminotransferase, total bilirubin, platelet count, albumin levels were demonstrated in all the patients. T-test, chi-squared test and logistic regression was used for analyzing data. Diagnostic efficiency and cut-off value of PIVKA-II in PVTT development of HCC patients were calculated using receiver operator curve (ROC) analysis.ResultsSerum level of PIVKA-II in HCC patients with PVTT was significantly higher than that in HCC patients without PVTT (995.8 mAU/ml vs 94.87 mAU/ml; P = 0.003), as well as D-dimer levels (2.12 mg/L vs 0.56 mg/L P = 0.001). Univariate analysis showed that high serum D-dimer level was an independent risk factor for development of PVTT (OR = 1.22, 95%CI 1.02–1.45). ROC curve showed that among analysis group, the area under ROC curve (AUROC) of PIVKA-II was 0.73 (95%CI 0.59–0.86). For the detection of PVTT in HCC, PIVKA-II had a sensitivity of 83.7% and a specificity of 69.2% at a cutoff of 221.26 mAU/ml, which had a sensitivity of 85.71% and a specificity of 55.56% in validation group, respectively.ConclusionSerum PIVKA-II level is a potential marker for diagnosis of PVTT in HCC patients, which may guide therapeutic strategy and assessment of tumor prognosis of HCC.

Highlights

  • As the fifth most common cancer and the second highest cause of cancer-related death, hepatocellular carcinoma (HCC) is a severe health problem all over the world [1]

  • Prothrombin induced by vitamin K absence-II (PIVK A-II) is a prothrombin (PT) precursor with no coagulation activity secreted from HCC cells, and it has been shown to be a predictor of microvascular invasion (MVI) [5, 6]

  • Baseline characteristics and comparison of PIVKA-II levels in analysis group and validation group Thirty-five HCC patients with portal vein tumor thrombosis (PVTT) and 88 HCC patients without PVTT were enrolled in the present study between March 2016 and October 2018

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Summary

Introduction

As the fifth most common cancer and the second highest cause of cancer-related death, hepatocellular carcinoma (HCC) is a severe health problem all over the world [1]. Serum levels of PIVKA-II have been demonstrated significantly increased in HCC patients and employed as a diagnostic marker in Asia [6, 7]. Several studies have revealed that PIVKA-II serum levels were significantly elevated in Eastern and European HCC patients [6, 8]. Higher PIVKA-II tissue expression was detected in HCC with microvascular invasion (MVI), as well as in serum [6]. It could be employed as a predictor of microvascular invasion [6]. The role of PIVK A-II in the development of macrovascular invasion such as PVTT is not well demonstrated

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