Woodhams B J, Than T, Than T, Hutton R A
Katharine Dormandy Haemophilia Centre, Royal Free Hospital, London, U.K.
Br J Haematol. 1989 Jan;71(1):107-11. doi: 10.1111/j.1365-2141.1989.tb06282.x.
Envenoming by Russell's viper caused a marked rise in FPA, B beta 15-42 fragment and fibrin derived cross-linked D-dimer fragment indicative of a consumptive coagulopathy with hyperfibrinolysis. There was no increase in tPA or tPA-I levels post envenoming, which suggests that the increase in fibrinolytic activity was not due to venom-induced release of tPA from the vessel walls but may have been attributable to a direct effect of the venom or to a secondary physiological response to fibrin deposition. The effectiveness of the antivenom is demonstrated by its ability to prevent further cleavage of fibrinogen and the return to normal fibrinogen levels by 24 h. A secondary rise in FPA at this time indicates that the initial dose of antivenom may have been too small. The antivenom alone or in combination with the venom causes the release of tPA, tPA-I and vWF by the vessel walls. This may be a consequence of the severe anaphylactic reactions seen in some patients.
罗素蝰蛇咬伤导致纤维蛋白肽A（FPA）、Bβ15 - 42片段和纤维蛋白衍生的交联D - 二聚体片段显著升高，提示存在伴有高纤维蛋白溶解的消耗性凝血病。咬伤后组织型纤溶酶原激活物（tPA）或tPA抑制物（tPA - I）水平没有升高，这表明纤溶活性的增加并非由于毒液诱导血管壁释放tPA，而可能归因于毒液的直接作用或对纤维蛋白沉积的继发生理反应。抗蛇毒血清的有效性体现在其能够防止纤维蛋白原进一步裂解，并在24小时内使纤维蛋白原水平恢复正常。此时FPA再次升高表明初始抗蛇毒血清剂量可能过小。单独使用抗蛇毒血清或与毒液联合使用会导致血管壁释放tPA、tPA - I和血管性血友病因子（vWF）。这可能是一些患者出现严重过敏反应的结果。
