This letter highlights the potential risk of intravascular coagulation with platelet transfusion in patients with antiplatelet antibodies and proposes delayed clearance as the mechanism for elevated antibodies post-splenectomy.
I read with interest the paper of Fuse et al. [1]in a recent issue of Acta Haematologica. Although some functional changes in platelets in idiopathic thrombocytopenic purpura (ITP) caused by antiplatelet antibodies (APA) [2, 3, 4]are expected, to my surprise APA to glycoprotein IIb did cause thrombasthenia without thrombocytopenia following splenectomy in the authors’ patient, though glycoprotein IIb and IIIa antibodies are frequent APA in ITP [5]. The authors stated that ‘the bruising finally was stopped by platelet concentrate transfusion’. Although possibly some decrease in the platelet-associated immunoglobulin G (PA IgG) level occurred with platelet transfusion [1;]fig. 1], their findings that ‘the normal platelets suspended in the patient’s PPP [platelet poor plasma] did not respond’ to ADP aggregation [1; fig. , 4]do not support their first statement. Actually platelet transfusion is potentially dangerous in the presence of APA, since it might cause intravascular coagulation though I have not seen clinical evidence of it yet.The authors statement ‘overproduction of antiplatelet antibody against glycoprotein IIb after splenectomy’ [1;]table 1] could also be the result of a clearance delay of it, since the spleen is the major site of destruction of platelets bound to APAs. Because the spleen is also the major site of production for APAs [6, 7], I would rather consider delayed clearance of APAs following splenectomy as the explanation for the elevated levels of glycoprotein IIb antibodies in the authors’ patient.
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Şînasi Özsoylu (1998) studied this question.
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