We thank Pivalizza et al. for their interest in our article and comments. They are correct that loading doses of antiplatelet agents are usually used in the context of revascularization procedures and acute ischemic events. However, we chose a more cautious approach because of the paucity of data regarding the use of antiplatelet agents in liver disease, especially in the context of ongoing anticoagulation with warfarin. To clarify the labeling of the traces in Fig. of our article, we note that these traces are related to arachidonic acid inhibition, which is denoted by the label MA AA .
When the patient started bleeding after the administration of tirofiban, fresh frozen plasma was chosen instead of a platelet transfusion because, even though the R time was shorter than that of previous traces, it was still prolonged at 9.2 minutes (normal R time ΒΌ 2-8 minutes), and the degree of platelet inhibition (70%) was less than that of the previous trace when the patient was not bleeding (100%). We were reluctant to counteract the antiplatelet therapy because of the likely mechanism of thrombosis for patients with Budd-Chiari syndrome.
We too are hopeful that the use of point-of-care monitors such as Thrombelastograph and Platelet-Mapping will lead to further insights into the mechanisms of thrombosis in liver disease, especially because of the limited utility of conventional tests. 2