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缺乏各种调节凝血机制的蛋白质,诸如抗凝血酶Ⅲ、纤维蛋白溶酶原、C蛋白和S蛋白,可引起一组征候群,称之为家族性高凝状态,其中C蛋白是1960年由Mammen首先发现,并于1976年由Stenflo命名,后来它也称为不活跃型的自身凝血酶原IIA.1981年Griffen首先对C蛋白缺乏症进行了临床研究.本文作者报道了5例C蛋白缺乏症,4例发生下肢深静脉血栓形成,1例患有肠系膜静脉血栓形成和小肠坏死.患者的年龄为28～41岁.2例的下肢静脉血栓形成反复发作,1例出现静脉郁滞性溃疡,1例出现肺栓塞.1例肠系膜静脉血栓形成患者系女性,28岁,口服避孕药,主诉恶心、呕吐和进行性剑突下腹痛已2天,在外施行剖腹探查,证实为肠系膜血栓形成,除近端30cm外,全部空肠坏死,切除坏死
The lack of a variety of proteins that regulate coagulation mechanisms, such as antithrombin III, plasminogen, protein C, and protein S, can cause a group of syndromes called familial hypercoagulable states, of which protein C was 1960 It was first discovered by Mammen and named after Stenflo in 1976, and later it was also referred to as inactive self-prothrombin IIA. Griffen first conducted a clinical study of protein deficiency in 1981. The authors reported five cases of protein C 4 cases developed deep venous thrombosis of the lower extremity, 1 had mesenteric venous thrombosis and necrosis of the small intestine.The age of the patients was 28 to 41 years old, 2 cases of recurrent venous thrombosis and 1 case of venous stasis 1 case of pulmonary embolism, 1 case of mesenteric venous thrombosis in women, 28 years old, oral contraceptives, nausea, vomiting and progressive hypoglossalgia for 2 days, external laparotomy proved mesentery thrombosis , Except for the proximal 30cm, all jejunal necrosis, removal of necrosis