Maruyama Shigeo, Matono Tomomitsu, Koda Masahiko
Maruyama Medical Clinic, Aioi-cho 3921, Hamada 697-0034, Shimane, Japan.
Department of Gastroenterology, Hyogo Prefectural Harima-Himeji General Hospital, Kamiya-cho 364, Himeji 670-8560, Hyogo, Japan.
Int J Mol Sci. 2025 Apr 13;26(8):3681. doi: 10.3390/ijms26083681.
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 ( < 0.0001), and significantly higher in the large hemangioma group ( < 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 ( < 0.0001) and all coagulation factors ( < 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.
关于肝血管瘤对维生素K缺乏或拮抗剂II诱导蛋白（PIVKA-II）的影响，目前所知甚少。本研究的目的是阐明PIVKA-II水平与肝血管瘤之间的相关性。在335例连续的肝血管瘤患者中，检查了超声（US）、肝功能实验室检查、血清PIVKA-II和甲胎蛋白（AFP）水平以及作为凝血障碍指标的凝血因子（血小板、凝血酶原时间（PT）、纤维蛋白原、凝血酶-抗凝血酶III复合物（TAT）、D-二聚体以及纤维蛋白和纤维蛋白原降解产物（FDPs））。血管瘤组的PIVKA-II水平显著高于对照组（<0.0001），在大血管瘤组中也显著更高（<0.0001）。血管瘤增大组的PIVKA-II水平随肿瘤大小和异常凝血因子的增加而升高，而血管瘤缩小组的PIVKA-II水平随肿瘤大小和异常凝血因子的降低而降低。PIVKA-II水平与肿瘤大小（<0.0001）以及除凝血酶原外的所有凝血因子（<0.05）均显著相关。肝血管瘤与血清PIVKA-II水平升高有关，与肿瘤大小和凝血障碍显著相关。PIVKA-II升高归因于血管瘤内加速的凝血-纤溶导致凝血酶原前体产生增加。
