Dargaud Yesim, Scoazec Jean Yves, Wielders Simone J H, Trzeciak Christine, Hackeng Tilman M, Négrier Claude, Hemker H Coenraad, Lindhout Theo, Castoldi Elisabetta
Unité d'Hémostase Clinique, Hôpital Cardiologique Louis Pradel, University Lyon I, France;
Laboratoire d'Anatomie Pathologique, Hôpital Edouard Herriot, Lyon, France;
Blood. 2015 Feb 26;125(9):1497-501. doi: 10.1182/blood-2014-10-604553. Epub 2015 Jan 6.
We describe a family with an autosomal dominant disorder characterized by severe trauma- and surgery-related bleeding. The proband, who experienced life-threatening bleeding during a routine operation, had normal clotting times, but markedly reduced prothrombin consumption. Plasma levels of all coagulation factors and of the main coagulation inhibitors were normal. Thrombin generation at low triggers was severely impaired and mixing experiments suggested the presence of a coagulation inhibitor. Using whole exome sequencing, the underlying genetic defect was identified as the THBD c.1611C>A mutation (p.Cys537Stop), which predicts a truncated form of thrombomodulin that is shed from the vascular endothelium. The patient had decreased expression of endothelium-bound thrombomodulin, but extremely elevated levels of soluble thrombomodulin in plasma, impairing the propagation phase of coagulation via rapid activation of protein C and consequent inactivation of factors Va and VIIIa. The same thrombomodulin mutation has been recently described in an unrelated British family with strikingly similar features.
我们描述了一个患有常染色体显性疾病的家族,其特征为与严重创伤和手术相关的出血。先证者在一次常规手术中经历了危及生命的出血,其凝血时间正常,但凝血酶原消耗显著减少。所有凝血因子和主要凝血抑制剂的血浆水平均正常。低触发条件下的凝血酶生成严重受损,混合实验提示存在一种凝血抑制剂。通过全外显子组测序,发现潜在的基因缺陷为THBD基因c.1611C>A突变(p.Cys537Stop),该突变预测会产生一种从血管内皮脱落的截短形式的血栓调节蛋白。患者血管内皮结合的血栓调节蛋白表达降低,但血浆中可溶性血栓调节蛋白水平极高,通过快速激活蛋白C以及随后使因子Va和VIIIa失活,损害了凝血的传播阶段。最近在一个具有显著相似特征的无关英国家族中也描述了相同的血栓调节蛋白突变。