Her platelet count decreased (41,000/μL) significantly and dabigatran treatment was discontinued. Therefore, warfarin treatment was replaced with dabigatran (300 mg/day). However, she had a new cerebral infarction. A 75-year-old woman had taken warfarin continuously for 8 years. The results of a blood test, performed 14 days after stopping dabigatran treatment, showed that the platelet count had recovered to the normal range of more than 150,000/μL. This suggested that dabigatran had caused thrombocytopenia and purpura therefore, dabigatran administration was discontinued. He was administered dabigatran (220 mg/day) for cerebral infarction for three days and his platelet count decreased abruptly (6000/μL).
A 73-year-old man showed hemorrhagic necrotic skin lesions on his neck and right hand. In this report, we discuss two cases of thrombocytopenia and purpura after dabigatran treatment. Thus, an antidote for dabigatran was developed to prevent thrombocytopenia. A few studies, however, reported that dabigatran can cause thrombocytopenia, although the underlying mechanism remains unclear. The major advantage of dabigatran, a direct thrombin inhibitor, is that it reversibly inhibits both free and clot-bound thrombin by tight binding affinity and the predictable pharmacodynamic effect. Novel oral anticoagulants (NOACs), such as dabigatran, are significantly safer in preventing thromboembolism than warfarin and heparin (sporadically causes thrombocytopenia) and are more specific for their target protein, thrombin. However, their administration is associated with a risk of bleeding and requires careful monitoring of patients. These agents have been mainstays of anticoagulation for people older than 60 years. myocardial infarction, venous thromboembolism, and stroke). heparin) are widely used to prevent thromboembolic disorders (e.g. warfarin) and indirect thrombin inhibitors (e.g.
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