Gonzales Mia, Pipalia Amrish, Weil Andrew
1 East Carolina University, Greenville, NC, USA.
2 Vidant Medical Center, Greenville, NC, USA.
J Investig Med High Impact Case Rep. 2019 Jan-Dec;7:2324709619832324. doi: 10.1177/2324709619832324.
Heparin-induced thrombocytopenia (HIT) type II is caused by antibody production that bind complexes between heparin and platelet factor 4 leading to platelet consumption and thrombosis. In a small subset of cases referred to as autoimmune HIT, the antibodies activate platelets even in the absence of heparin. Refractory HIT is a type of autoimmune HIT in which thrombocytopenia persists for weeks after heparin discontinuation and carries increased risk for thrombosis and more severe thrombocytopenia. We present a case of refractory HIT with cerebral venous sinus thrombosis (CVST) that was successfully treated with a change in anticoagulant alongside steroids and a second trial of intravenous immunoglobulin (IVIg).
II型肝素诱导的血小板减少症(HIT)是由抗体产生引起的,这些抗体结合肝素与血小板因子4之间的复合物,导致血小板消耗和血栓形成。在一小部分被称为自身免疫性HIT的病例中,即使在没有肝素的情况下,抗体也会激活血小板。难治性HIT是一种自身免疫性HIT,其中血小板减少症在停用肝素后持续数周,并伴有血栓形成风险增加和更严重的血小板减少症。我们报告一例难治性HIT合并脑静脉窦血栓形成(CVST)的病例,该病例通过更换抗凝剂、联合使用类固醇以及再次静脉注射免疫球蛋白(IVIg)成功得到治疗。