THE RATE OF FIBRINOPEPTIDE-B RELEASE MODULATES THE RATE OF CLOT FORMATION - A STUDY WITH AN ACQUIRED INHIBITOR TO FIBRINOPEPTIDE-B RELEASE
THE RATE OF FIBRINOPEPTIDE-B RELEASE MODULATES THE RATE OF CLOT FORMATION - A STUDY WITH AN ACQUIRED INHIBITOR TO FIBRINOPEPTIDE-B RELEASE
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DOI：
10.1111/j.1365-2141.1991.tb04536.x
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发表时间：
1991-10-01
影响因子：
6.5
通讯作者：
SCHMAIER, AH
中科院分区：
文献类型：
--
作者：
NAWARAWONG, W;WYSHOCK, E;SCHMAIER, AH
一名无症状的50岁男性与丙种球蛋白副蛋白被发现，有延长凝血酶原时间，活化部分凝血活酶时间，凝血酶时间，但正常的立止血时间。 凝血时间延长不是因子缺乏的结果，因为它们不能通过加入正常血浆来纠正。 相反，该患者具有延迟凝血酶介导的纤维蛋白肽B释放的抗体，从而产生明显的异常纤维蛋白原血症。 他分离的IgG延长了正常血浆和纤维蛋白原的凝血酶凝固时间。 将His IgG与纤维蛋白肽B预孵育，但不与纤维蛋白肽A或凝血酶预孵育，降低了其延长凝血酶凝血时间的能力。 患者的纯化IgG而非对照IgG延迟凝血酶介导的纤维蛋白肽B从纤维蛋白原的释放，而不影响纤维蛋白肽A的释放。 这些研究定义了一种新型的、临床上无症状的异常纤维蛋白原血症，其归因于一种抗体，该抗体延迟凝血酶介导的纤维蛋白肽B从纤维蛋白原释放，从而显著延长凝血时间。
An asymptomatic 50-year-old male with a gamma globulin paraprotein was found, to have prolonged prothrombin time, activated partial thromboplastin time, and thrombin time but a normal reptilase time. The prolonged clotting times were not the result of a factor deficiency because they were not corrected by the addition of normal plasma. Instead, this patient had an antibody that delayed thrombin-mediated fibrinopeptide B release thereby producing an apparent dysfibrinogenaemia. His isolated IgG prolonged the thrombin clotting time of both normal plasma and fibrinogen. Precincubation of his IgG with fibrinopeptide B, but not with fibrinopeptide A or thrombin, decreased its ability to prolong the thrombin clotting time. The patient's purified IgG but not control IgG delayed thrombin-mediated fibrinopeptide B release from fibrinogen without affecting the release of fibrinopeptide A. These studies define a novel, clinically silent dysfibrinogenaemia due to an antibody that delays thrombin-mediated fibrinopeptide B release from fibrinogen thereby markedly prolonging the clotting times.