Elevated Serum Protein Induced by Vitamin K Absence or Antagonist II Levels in Patients with Hepatic Hemangiomas

肝血管瘤患者血清蛋白升高是由维生素K缺乏或拮抗剂II水平升高引起的

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Abstract

Little is known about the effect of hepatic hemangiomas on protein induced by vitamin K absence or antagonist II (PIVKA-II). The aim of this study was to clarify the correlation of PIVKA-II levels with hepatic hemangiomas. In 335 consecutive patients with hepatic hemangiomas, ultrasonography (US), laboratory tests for liver function, serum levels of PIVKA-II and α-fetoprotein (AFP), and coagulation factors (platelets, prothrombin time (PT), fibrinogen, thrombin-antithrombin III complex (TAT), D-dimer, and fibrin and fibrinogen degradation products (FDPs)) as indicators of coagulation disorders were examined. PIVKA-II levels were significantly higher in the hemangioma group than in the control group (p < 0.0001), and significantly higher in the large hemangioma group (p < 0.0001). PIVKA-II levels in the hemangioma increase group were higher with increases in tumor size and abnormal coagulation factors, and those in the hemangioma decrease group were lower with decreases in tumor size and abnormal coagulation factors. PIVKA-II levels were significantly correlated with tumor size (p < 0.0001) and all coagulation factors (p < 0.05) except prothrombin. Hepatic hemangiomas were associated with elevated serum PIVKA-II levels, showing significant correlations with tumor size and coagulation disorders. PIVKA-II elevation was attributed to the increased production of prothrombin precursors caused by accelerated coagulation-fibrinolysis within hemangiomas.

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