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Graft-v-host disease is associated with autoimmune-like thrombocytopenia
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C Anasetti, W Rybka, KM Sullivan, M Banaji and SJ Slichter
Puget Sound Blood Center, Seattle, WA 98104.
Persistent thrombocytopenia after allogeneic marrow transplantation is
associated with poor patient survival. To identify the mechanisms of the
thrombocytopenia, we studied platelet and fibrinogen kinetics and
antiplatelet antibodies in 20 patients between 60 and 649 days (median 90)
after transplantation. Seventeen patients had isolated thrombocytopenia
(less than 100 X 10(9) platelets/L): the marrow cellularity was normal in
five patients and slightly reduced in 12, and there was no discrepancy
between thrombopoiesis and myeloerythropoiesis. Three patients had
pancytopenia following marrow graft rejection (two) and relapse of leukemia
(one). Only three patients had evidence of increased platelet production,
indicating that in most cases there is a poor marrow response to
thrombocytopenia early after marrow grafting. There was no correlation
between platelet count and splenic pooling, suggesting that hypersplenism
was an unlikely mechanism of the thrombocytopenia. Although there was a
direct relationship between platelet count and platelet survival, the
reduction in platelet survival was greater than what could be explained by
the fixed platelet removal found in thrombocytopenic patients; this
suggests increased platelet destruction. Seven patients had intercurrent
infections that reduced both platelet and fibrinogen survivals. In
addition, platelet antibodies bound to autologous or marrow donor platelets
were present in five of the 12 patients studied. Patients with antiplatelet
antibodies had lower platelet counts (30 +/- 10 X 10(9)/L v. 49.1 +/- 28.7
X 10(9)/L, P less than 0.05) and platelet survivals (1.32 +/- 0.92 days v.
3.58 +/- 2.02 days, P less than 0.05) than patients without antiplatelet
antibodies. Furthermore, platelet- bound autoantibodies were present in
five of six patients with grade II- IV acute or chronic graft-versus-host
disease (GVHD), but were not present in six patients free of GVHD (P less
than 0.01). We conclude that persistent thrombocytopenia after marrow
transplantation is most often secondary to increased platelet destruction
mediated by multiple mechanisms and that platelet autoantibodies are found
in patients with acute or chronic GVHD.
Volume 73,
Issue 4,
pp. 1054-1058,
03/01/1989
Copyright © 1989 by The American Society of Hematology
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