Platelet Function in a Family with Abnormal Antithrombin III-Toyama

Abstract

Deficincies and abnormalities of antithrombin III (AT III) are considered to be the very important pathogenesis of thrombosis. We have reported abnormal antithrombin III (AT III-Toyama), in ICTH (Toronto) in 1981. In our case the proband, 23 years-old female, happened to have cerebral thrombosis 5 days after the exploratory laparotomy performed to identify her abdominal tumor, and she experienced a transient and extreme thrombocytopenia at that time. In order to identify the cause of this thrombocytopenia, we investigated the platelet function of this family and found that the sensitivities of this family's platelets against ADP, collagen, epinephrine and thrombin were not significantly different from those of normal persons. And the suppressive effect of heparin against thrombin induced platelet aggregation of her platelet also was found to be almost normal. Therefore, the thrombocytopenia occurred at the time of apoplexy attack is considered to be caused not by the hypersensitivity of her platelet but by the defect of the patient's AT III to neutralize thrombin generated in her plasma.