Recurrent venous thrombosis as the presenting manifestation of acute lymphocytic leukemia: leukemic cell procoagulant activity is not responsible for the hypercoagulable state

The association of cancer with clinical abnormalities of blood coagulation, including superficial thrombophlebitis, deep vein thrombosis (DVT), and disseminated intravascular coagulation (DIC) is well-known, particularly in patients with solid tumors and acute promyelocytic leukemia (APL). Less comm...

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Published inMedical and pediatric oncology Vol. 24; no. 1; p. 40
Main Authors Bilgrami, S, Greenberg, B R, Weinstein, R E, Hair, G A, Rickles, F R
Format Journal Article
LanguageEnglish
Published United States 01.01.1995
Subjects
Adult
Blood Coagulation Factors - analysis
Blotting, Northern
Burkitt Lymphoma - diagnosis
Burkitt Lymphoma - metabolism
Cysteine Endopeptidases - analysis
Humans
Male
Middle Aged
Neoplasm Proteins
RNA, Messenger - analysis
Thrombophlebitis - diagnosis
Thromboplastin - genetics
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Summary:The association of cancer with clinical abnormalities of blood coagulation, including superficial thrombophlebitis, deep vein thrombosis (DVT), and disseminated intravascular coagulation (DIC) is well-known, particularly in patients with solid tumors and acute promyelocytic leukemia (APL). Less commonly appreciated is the potential for the development of venous thromboembolic disease (TED) in patients with acute lymphocytic leukemia (ALL). Multiple mechanisms have been implicated for the activation of coagulation in these patients, with an emphasis on the contribution made by the procoagulant properties of the tumor cells themselves. We present two cases of patients with pre-B cell ALL, both of whom developed recurrent TED as the presenting manifestation of their leukemia and/or heralding relapse. The blast cells from one of the patients were studied for the presence of procoagulant activity (PCA) and by Northern blot analysis for tissue factor (TF) messenger RNA (mRNA). Neither PCA nor TF mRNA could be identified in highly purified populations of the lymphoblast cells. We conclude that recurrent TED can be a manifestation of ALL and that mechanisms other than the release of tumor cell procoagulants should be sought to explain the pathogenesis of thrombosis in some patients.
ISSN:0098-1532
DOI:10.1002/mpo.2950240109