Nakano Y, Sato A, Okano A, Chida K, Yasumi T
Second Department of Internal Medicine, Hamamatsu University School of Medicine, Shizuoka, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1993 Feb;31(2):214-8.
We present a 36-year-old male who developed pulmonary infarction secondary to antithrombin III variant. He was admitted to our hospital with progressive chest pain and hemosputum. The presence of multiple defects on 99mTc perfusion scan indicated the diagnosis of pulmonary infarction. He had a past history of pulmonary infarction 4 years before this episode as well as a family history of recurrent thromboembolic disease. Through coagulation studies revealed that the concentration of antithrombin III antigen and progressive antithrombin activity were within normal limits, while heparin cofactor activity was decreased markedly. Of 5 people in his family, 4 proved to have low heparin cofactor activity. These data suggest that functional abnormality of antithrombin III seems to be closely associated with pulmonary infarction.
我们报告一名36岁男性,其因抗凝血酶III变异继发肺梗死。他因进行性胸痛和咯血入住我院。99mTc灌注扫描显示多个缺损,提示肺梗死诊断。他在此次发作前4年有肺梗死病史,且有复发性血栓栓塞性疾病家族史。凝血研究显示,抗凝血酶III抗原浓度和抗凝血酶活性正常,而肝素辅因子活性明显降低。他家族中的5人中有4人肝素辅因子活性较低。这些数据表明,抗凝血酶III的功能异常似乎与肺梗死密切相关。