Zeller J A, Schlesinger S, Runge U, Kessler C
Department of Neurology, University of Kiel, Germany.
Epilepsia. 1999 Feb;40(2):186-9. doi: 10.1111/j.1528-1157.1999.tb02073.x.
Valproate (VPA) has been linked to coagulation disturbances, with both impaired and exaggerated clotting, which has been attributed to an effect of VPA on platelets or hemostatic proteins. Additional thrombocytic function testing may help to identify patients at risk of increased bleeding caused by platelet dysfunction.
We evaluated the influence of VPA on hematologic routine values and platelet activation by using immunostaining and flow cytometry in 30 patients receiving long-term VPA therapy and in 30 controls.
The fraction of activated platelets was similar in both groups; however, the general extent of platelet activation was significantly lower in the patient group, with considerable interindividual variability. In addition, patients had a significantly lower platelet count, prolonged thrombin time, and higher mean corpuscular hemoglobin.
Our data confirm the previously reported hematologic changes caused by VPA and additionally suggest that VPA impairs procoagulatory thrombocytic function, which is reflected by reduced platelet activation and increased thrombin time. Possible mechanisms of VPA-platelet interaction are discussed.
丙戊酸盐(VPA)与凝血紊乱有关,既有凝血功能受损,也有凝血功能亢进,这归因于VPA对血小板或止血蛋白的影响。额外的血小板功能检测可能有助于识别因血小板功能障碍而有出血增加风险的患者。
我们通过免疫染色和流式细胞术评估了VPA对30例接受长期VPA治疗的患者和30例对照者血液学常规值和血小板活化的影响。
两组中活化血小板的比例相似;然而,患者组血小板活化的总体程度显著较低,个体间存在相当大的变异性。此外,患者的血小板计数显著降低,凝血酶时间延长,平均红细胞血红蛋白较高。
我们的数据证实了先前报道的由VPA引起的血液学变化,并进一步表明VPA损害促凝血血小板功能,这表现为血小板活化减少和凝血酶时间延长。讨论了VPA与血小板相互作用的可能机制。