26 Citations (Scopus)

Abstract

A decrease in levels of circulating anticoagulant protein C has been shown to occur following autologous BMT, and this deficiency may contribute to a hypercoagulable state placing patients at risk for thromboembolic events. We report four patients who suffered a variety of thrombotic complications following BMT (non-bacterial thrombotic endocarditis, superior vena cava thrombosis, thrombotic stroke, purpura fulminans, small bowel infarction secondary to diffuse microvascular thrombosis), which were preceded by or temporally related to decreased levels of protein C. Treatment with fresh frozen plasma (FFP) led to slight, temporary increases in protein C levels but infusions of FFP did not prevent either death or extension of the thrombus in these four cases, suggesting the need for higher protein C doses and/or concomitant anticoagulation. Though no direct causal relationship between these thrombotic complications and the protein C deficiency can be proved, a generalized hypercoagulable state caused by protein C deficiency may have contributed to the development, severity or progression of these complications.

Original languageEnglish (US)
Pages (from-to)61-65
Number of pages5
JournalBone marrow transplantation
Volume11
Issue number1
StatePublished - Jan 1 1993

Fingerprint

Protein C Deficiency
Protein C
Non-Infective Endocarditis
Thrombosis
Purpura Fulminans
Superior Vena Cava Syndrome
Infarction
Stroke

ASJC Scopus subject areas

  • Hematology
  • Transplantation

Cite this

Thrombotic complications of BMT : Association with protein C deficiency. / Gordon, B. G.; Haire, W. D.; Patton, D. F.; Manno, P. J.; Reed, E. C.

In: Bone marrow transplantation, Vol. 11, No. 1, 01.01.1993, p. 61-65.

Research output: Contribution to journalArticle

Gordon, B. G. ; Haire, W. D. ; Patton, D. F. ; Manno, P. J. ; Reed, E. C. / Thrombotic complications of BMT : Association with protein C deficiency. In: Bone marrow transplantation. 1993 ; Vol. 11, No. 1. pp. 61-65.
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AU - Gordon, B. G.

AU - Haire, W. D.

AU - Patton, D. F.

AU - Manno, P. J.

AU - Reed, E. C.

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N2 - A decrease in levels of circulating anticoagulant protein C has been shown to occur following autologous BMT, and this deficiency may contribute to a hypercoagulable state placing patients at risk for thromboembolic events. We report four patients who suffered a variety of thrombotic complications following BMT (non-bacterial thrombotic endocarditis, superior vena cava thrombosis, thrombotic stroke, purpura fulminans, small bowel infarction secondary to diffuse microvascular thrombosis), which were preceded by or temporally related to decreased levels of protein C. Treatment with fresh frozen plasma (FFP) led to slight, temporary increases in protein C levels but infusions of FFP did not prevent either death or extension of the thrombus in these four cases, suggesting the need for higher protein C doses and/or concomitant anticoagulation. Though no direct causal relationship between these thrombotic complications and the protein C deficiency can be proved, a generalized hypercoagulable state caused by protein C deficiency may have contributed to the development, severity or progression of these complications.

AB - A decrease in levels of circulating anticoagulant protein C has been shown to occur following autologous BMT, and this deficiency may contribute to a hypercoagulable state placing patients at risk for thromboembolic events. We report four patients who suffered a variety of thrombotic complications following BMT (non-bacterial thrombotic endocarditis, superior vena cava thrombosis, thrombotic stroke, purpura fulminans, small bowel infarction secondary to diffuse microvascular thrombosis), which were preceded by or temporally related to decreased levels of protein C. Treatment with fresh frozen plasma (FFP) led to slight, temporary increases in protein C levels but infusions of FFP did not prevent either death or extension of the thrombus in these four cases, suggesting the need for higher protein C doses and/or concomitant anticoagulation. Though no direct causal relationship between these thrombotic complications and the protein C deficiency can be proved, a generalized hypercoagulable state caused by protein C deficiency may have contributed to the development, severity or progression of these complications.

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