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摘要
Budd-Chiari syndrome (BCS) is the end result of a number of disease states resulting in hepatic venous outflow obstruction. We report a Janus kinase 2-homozygous patient with BCS who thrombosed a transjugular intrahepatic portosystemic shunt (TIPS) despite treatment with warfarin (international normalized ratio = 3.0), aspirin, and clopidogrel. PlateletMapping (TM) (Haemonetics Corp.) is a novel point-of-care assay of platelet function based on thromboelastography (TEG) that has the ability to detect platelet inhibition (%) by antiplatelet therapy. Initial PlateletMapping (TM) traces showed no platelet inhibition by aspirin or clopidogrel but demonstrated adequate suppression of plasmatic coagulation. On this basis, the aspirin dose was doubled, and this resulted in a significant increase in platelet inhibition (45%). To further suppress platelet activity, the patient was started on tirofiban, a glycoprotein IIb/IIIa inhibitor. Repeat PlateletMapping (TM) revealed 100% inhibition of platelets by both pathways, and this coincided with angiographic evidence of TIPS blood flow. Subsequently, the patient developed bleeding from the venous access sites. TEG demonstrated poor underlying plasmatic coagulation with a prolonged R time of 9.2 minutes (normal = 2-8 minutes), and the international normalized ratio was found to be supratherapeutic (> 4). Treatment with fresh frozen plasma stopped the bleeding without compromising the platelet inhibition. This case demonstrates that increased platelet activation may contribute to the development of thromboses in BCS. Despite the standard dose of dual antiplatelet therapy, there was minimal inhibition in platelet function, and anticoagulation with warfarin alone was not adequate to prevent thrombotic events. PlateletMapping (TM) was used to assess and then optimize the antiplatelet treatment while facilitating the management of complications without an increased risk of thrombosis. Liver Transpl 16:38-41, 2010.
- 出版日期2010-1
