先天性凝血因子X缺乏是少见病,只占人口的50万分之一,是按常染色体隐性遗传的,本病至今文献已报导近30例。Stuart-Prower病的命名是根据第一次发现的两名患者的名字,其临床表现为粘膜、伤口或手术后出血不止,但关节出血很少。实验室检查为凝血酶原活动度下降,往往与因子Ⅶ缺乏相似。因子Ⅹ和Ⅶ缺乏的鉴别,在目前的检查方法中还比较困难。但是如果正确地了解因子Ⅹ在凝血过程中的作用,诊断其缺乏可以无误。因子Ⅹ是以不活泼状态存在于血浆中,当血液凝固时,在钙参加下通过两个途径可激活。一个是组织凝血活酶和Ⅶ因子互相作用的产物(组织系统凝血活酶生成),另一个是因子Ⅸ、Ⅷ和血小板磷脂互相作用的 Congenital clotting factor X deficiency is a rare disease, only one half of the population of one million, is based on autosomal recessive inheritance, the disease has been reported in the literature so far nearly 30 cases. The Stuart-Prower disease is named after the first two patients who were found to have a clinical appearance of mucosal wounds or more bleeding after surgery or surgery but with little joint bleeding. Laboratory tests for prothrombin activity decreased, often with the lack of similar factors VII. The lack of identification of factors X and VII is still more difficult in the current test methods. However, a correct diagnosis of the absence of factor X is correct if it is properly understood. Factor X is present in the plasma in an inactive state, and when blood coagulates it is activated by two pathways with calcium participation. One is the product of the interaction between thromboplastin and factor VII (tissue system thromboplastin production) and the other is the interaction between factor IX, VIII and platelet phospholipids