[A case of recurrent pulmonary thromboembolism presenting with positive antiphospholipid antibodies].

A 76-year-old man was admitted to our hospital in December of 1990, for investigation of progressive dyspnea on exertion over the previous 3 months. Physical examination revealed cyanosis, but no edema. Cardiomegaly was seen on chest X-ray, and findings compatible with right-sided congestive heart failure were revealed by ECG and echocardiography. Lung perfusion scintigrams showed multiple defects in both lungs, but no abnormal findings were detected on a ventilation study. Venograms of the lower extremities disclosed thrombosis of the right femoral vein. Therefore, a diagnosis of recurrent pulmonary thromboembolism was made. Furthermore, lupus anticoagulant and IgG-class anticardiolipin antibody were noted in the serum. The patient was treated with intravenous heparin, long-term warfarin, and transvenous placement of a Greenfield filter in the inferior vena cava. The clinical symptoms and signs improved, and no recurrence has been seen during the 13 months since the onset. On discharge, both antiphospholipid antibodies were negative. This case of primary antiphospholipid syndrome without autoimmune disease, with transiently positive antibodies only in the exacerbation phase, is discussed herein.

[A case of familial antithrombin III variant complicated by recurrent pulmonary infarction].

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.