Wilde J T, Thomas W E, Lane D A, Greaves M, Preston F E
University Department of Haematology, Royal Hallamshire Hospital, Sheffield.
J Clin Pathol. 1988 Jun;41(6):615-8. doi: 10.1136/jcp.41.6.615.
Acquired dysfibrinogenaemia as the cause of coagulation abnormalities occurred in a case of acute pancreatitis. Initial coagulation studies showed a prolonged thrombin time and increased concentrations of serum fibrinogen/fibrin degradation products and plasma D-dimer. Further studies on purified fibrinogen showed evidence of degradation of the C-terminal ends of the A-alpha chains, which, it is suggested, resulted from the action of circulating pancreatic proteases. Fibrin polymerisation was thus shown to be impaired, which explains the prolongation of the thrombin time. There was a temporal relation between increased amylase activities and the prolonged thrombin time, both of which returned to normal three weeks after admission. Acquired dysfibrinogenaemia may be an underrecognized phenomenon in acute pancreatitis and may lead to misinterpretation of coagulation test abnormalities.
一名急性胰腺炎患者出现获得性异常纤维蛋白原血症,这是凝血异常的原因。初始凝血研究显示凝血酶时间延长,血清纤维蛋白原/纤维蛋白降解产物和血浆D - 二聚体浓度升高。对纯化纤维蛋白原的进一步研究显示A-α链C末端有降解迹象,提示这是循环中胰腺蛋白酶作用的结果。由此表明纤维蛋白聚合受损,这解释了凝血酶时间延长的原因。淀粉酶活性升高与凝血酶时间延长之间存在时间关系,两者在入院三周后均恢复正常。获得性异常纤维蛋白原血症在急性胰腺炎中可能是一种未被充分认识的现象,可能导致对凝血试验异常的错误解读。