Graft-v-host disease is associated with autoimmune-like thrombocytopenia

C. Anasetti, Witold Rybka, K. M. Sullivan, M. Banaji, S. J. Slichter

Research output: Contribution to journalArticle

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Abstract

Persistent thrombocytopenia after allogenic 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 (< 100 x 109 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 thrombopenic 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 109/L v. 49.1 ± 28.7 x 109/L, P < 0.05) and platelet survivals (1.32 ± 0.92 days v. 3.58 ± 2.02 days, P < 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 < 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.

Original languageEnglish (US)
Pages (from-to)1054-1058
Number of pages5
JournalBlood
Volume73
Issue number4
StatePublished - Jan 1 1989

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Idiopathic Thrombocytopenic Purpura
Platelets
Grafts
Blood Platelets
Transplants
Thrombocytopenia
Bone Marrow
Graft vs Host Disease
Platelet Count
Antibodies
Autoantibodies
Fibrinogen
Transplantation
Hypersplenism
Thrombopoiesis
Pancytopenia
Homologous Transplantation
Graft Rejection

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

Anasetti, C., Rybka, W., Sullivan, K. M., Banaji, M., & Slichter, S. J. (1989). Graft-v-host disease is associated with autoimmune-like thrombocytopenia. Blood, 73(4), 1054-1058.
Anasetti, C. ; Rybka, Witold ; Sullivan, K. M. ; Banaji, M. ; Slichter, S. J. / Graft-v-host disease is associated with autoimmune-like thrombocytopenia. In: Blood. 1989 ; Vol. 73, No. 4. pp. 1054-1058.
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abstract = "Persistent thrombocytopenia after allogenic 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 (< 100 x 109 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 thrombopenic 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 109/L v. 49.1 ± 28.7 x 109/L, P < 0.05) and platelet survivals (1.32 ± 0.92 days v. 3.58 ± 2.02 days, P < 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 < 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.",
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Anasetti, C, Rybka, W, Sullivan, KM, Banaji, M & Slichter, SJ 1989, 'Graft-v-host disease is associated with autoimmune-like thrombocytopenia', Blood, vol. 73, no. 4, pp. 1054-1058.

Graft-v-host disease is associated with autoimmune-like thrombocytopenia. / Anasetti, C.; Rybka, Witold; Sullivan, K. M.; Banaji, M.; Slichter, S. J.

In: Blood, Vol. 73, No. 4, 01.01.1989, p. 1054-1058.

Research output: Contribution to journalArticle

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AB - Persistent thrombocytopenia after allogenic 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 (< 100 x 109 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 thrombopenic 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 109/L v. 49.1 ± 28.7 x 109/L, P < 0.05) and platelet survivals (1.32 ± 0.92 days v. 3.58 ± 2.02 days, P < 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 < 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.

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Anasetti C, Rybka W, Sullivan KM, Banaji M, Slichter SJ. Graft-v-host disease is associated with autoimmune-like thrombocytopenia. Blood. 1989 Jan 1;73(4):1054-1058.