Koenig Stephan, Gerstner Thorsten, Keller Anja, Teich Martin, Longin Elke, Dempfle Carl-Erik
Department of Pediatrics, Germany, Mannheim University Hospital, University of Heidelberg, Germany.
Blood Coagul Fibrinolysis. 2008 Jul;19(5):375-82. doi: 10.1097/MBC.0b013e3282f3f9ec.
Reports have been published on blood coagulation disturbances by valproate therapy. In the present prospective trial, blood samples were drawn before valproate therapy, after 6 weeks of therapy, after more than 6 weeks and after longer than 6 months of valproate therapy from 23 children newly treated with valproate. Two children developed thrombocytopenia, and six children with initial normal von Willebrand factor showed acquired von Willebrand's disease. Fibrinogen levels dropped below the lower limit in 12 patients and subnormal factor XIII plasma levels were observed in 17% of patients. No patient developed signs of hemorrhage. Eight percent of patients developed valproate-induced thrombocytopenia. Reduction in platelets did not reach statistic significance. Thrombelastography showed a 47% incidence of altered platelet function. We found a statistically significant, positive correlation between clotting time of collagen extrinsic pathway inhibitor and, accordingly, adenosindiphosphate and valproate level. Plasmatic coagulation investigations showed a significant decrease of prothrombin time. Activated partial thromboplastin time measurements also showed significant prolongation with valproate. Activity of von Willebrand factor antigen and von Willebrand factor ristocetin cofactor significantly decreased. Factor XIII activity significantly decreased after valproate therapy for longer than 6 months (17% of children). Fibrinogen was significantly reduced. In the coagulatory system a decrease in the main antiprotease antithrombin III activity was observed. Blood coagulation disturbances are common in patients with valproate, but rarely become clinically symptomatic. Acquired von Willebrand's disease and hypofibrinogenemia may become relevant in patients with surgery or trauma. Particular attention should be paid to factor-XIII deficiency, which is especially seen with valproate therapy.
已有关于丙戊酸盐治疗引起血液凝固紊乱的报道。在本前瞻性试验中,从23名新接受丙戊酸盐治疗的儿童中,在丙戊酸盐治疗前、治疗6周后、超过6周后以及超过6个月后采集血样。两名儿童出现血小板减少症,6名初始血管性血友病因子正常的儿童出现获得性血管性血友病。12名患者的纤维蛋白原水平降至下限以下,17%的患者观察到血浆因子XIII水平低于正常。没有患者出现出血迹象。8%的患者出现丙戊酸盐诱导的血小板减少症。血小板减少未达到统计学意义。血栓弹力图显示血小板功能改变的发生率为47%。我们发现胶原外源性途径抑制剂的凝血时间与二磷酸腺苷和丙戊酸盐水平之间存在统计学上显著的正相关。血浆凝血检查显示凝血酶原时间显著缩短。活化部分凝血活酶时间测量也显示丙戊酸盐治疗后显著延长。血管性血友病因子抗原和血管性血友病因子瑞斯托霉素辅因子的活性显著降低。丙戊酸盐治疗超过6个月后(17%的儿童),因子XIII活性显著降低。纤维蛋白原显著减少。在凝血系统中,观察到主要抗蛋白酶抗凝血酶III活性降低。丙戊酸盐治疗的患者中血液凝固紊乱很常见,但很少出现临床症状。获得性血管性血友病和低纤维蛋白原血症在手术或创伤患者中可能会变得重要。应特别注意因子XIII缺乏症,这在丙戊酸盐治疗中尤为常见。