Fisher M, Francis R
Department of Neurology, University of Southern California School of Medicine, Los Angeles 90033.
Arch Neurol. 1990 Oct;47(10):1075-9. doi: 10.1001/archneur.1990.00530100037011.
We investigated hemostatic function in patients with cerebral ischemia by evaluating platelet activation, fibrin generation, and fibrinolysis. Plasma beta-thromboglobulin, an index of platelet activation, was significantly increased both acutely (14.9 +/- 9.2 ng/mL; n = 85) and approximately 2 months later (17.3 +/- 10.1 ng/mL; n = 57). Thrombin activity was measured using assays for fibrinopeptide A and fibrin D-dimer. Increased fibrinopeptide A was found in 9 (11.5%) of 78 patients acutely and 6 (10.7%) of 56 at follow-up; fibrin D-dimer levels were significantly increased acutely (166 +/- 188 ng/mL; n = 66) but not at follow-up. Fibrinolytic activity was measured using assays for fibrinopeptide B-beta 1-42 and plasminogen activator inhibitor 1. Fibrinopeptide B-beta 1-42 was significantly reduced acutely (6.3 +/- 2.2 pmol/mL; n = 35) and at follow-up (4.8 +/- 1.5 pmol/mL; n = 21). Plasminogen activator inhibitor 1 was normal acutely (20.1 +/- 12.0 ng/mL; n = 73) but increased at follow-up (27.8 +/- 20.1 ng/mL; n = 45). These results demonstrate that patients with cerebral ischemia have abnormal hemostatic function that is not explained by the acute phase reaction, and that components of the prethrombotic state are present in some of these patients.
我们通过评估血小板活化、纤维蛋白生成和纤维蛋白溶解来研究脑缺血患者的止血功能。血浆β-血小板球蛋白作为血小板活化指标,在急性期(14.9±9.2 ng/mL;n = 85)和大约2个月后(17.3±10.1 ng/mL;n = 57)均显著升高。使用纤维蛋白肽A和纤维蛋白D-二聚体检测法测定凝血酶活性。急性时,78例患者中有9例(11.5%)纤维蛋白肽A升高,随访时56例中有6例(10.7%)升高;纤维蛋白D-二聚体水平在急性期显著升高(166±188 ng/mL;n = 66),但随访时未升高。使用纤维蛋白肽B-β1-42和纤溶酶原激活物抑制剂1检测法测定纤维蛋白溶解活性。纤维蛋白肽B-β1-42在急性期(6.3±2.2 pmol/mL;n = 35)和随访时(4.8±1.5 pmol/mL;n = 21)均显著降低。纤溶酶原激活物抑制剂1在急性期正常(20.1±12.0 ng/mL;n = 73),但随访时升高(27.8±20.1 ng/mL;n = 45)。这些结果表明,脑缺血患者具有异常的止血功能,这不能用急性期反应来解释,并且这些患者中的一些存在血栓前状态的成分。