2nd Department of Medicine, University of Debrecen, Debrecen, Hungary.
Platelets. 2012;23(6):495-8. doi: 10.3109/09537104.2011.650245. Epub 2012 Feb 6.
Heparin-induced thrombocytopenia (HIT) is one of the most common immune-mediated drug reactions. Immunoglobulin G-type antibodies against platelet factor 4(PF4)/heparin complexes are known to play a key role in the pathogenesis of HIT. Rapid-onset HIT is caused by the presence of circulating HIT antibodies at the time of heparin readministration. These antibodies are generally resulted from a recent immunizing exposure to heparin. Here we report a case of rapid-onset HIT developed after a septicemia without previous heparin exposure. The diagnosis of HIT as well as the presence of platelet activating and heparin-dependent antibodies was confirmed by ELISA and flow cytometric functional assays. Our case report reinforces that rapid-onset HIT cannot be excluded only based on the absence of previous heparin exposure. In addition, it may support the new theory of pre-immunization by PF4-coated bacteria in the pathomechanism of HIT. We also call the attention that venous limb gangrene can be rarely associated with HIT and thrombosis even in the absence of coumarin therapy. Furthermore, transient presence of anti-phospholipid antibodies can cause a differential diagnostic problem in the cases of HIT.
肝素诱导的血小板减少症(HIT)是最常见的免疫介导的药物反应之一。已知针对血小板因子 4(PF4)/肝素复合物的免疫球蛋白 G 型抗体在 HIT 的发病机制中起关键作用。快速发作的 HIT 是由于肝素再次给药时存在循环中的 HIT 抗体引起的。这些抗体通常是由于最近接触肝素而产生的免疫。在这里,我们报告了一例在没有先前肝素暴露的情况下发生的败血症后快速发作的 HIT。通过 ELISA 和流式细胞术功能测定确认了 HIT 的诊断以及血小板激活和肝素依赖性抗体的存在。我们的病例报告证实,仅根据没有先前肝素暴露,不能排除快速发作的 HIT。此外,它可能支持 HIT 发病机制中 PF4 包被细菌的预免疫新理论。我们还提醒注意,即使没有使用香豆素治疗,静脉肢体坏疽也可能与 HIT 和血栓形成很少相关。此外,抗磷脂抗体的短暂存在可能会导致 HIT 病例的鉴别诊断问题。