The coagulopathy of childhood leukemia thrombin activation or primary fibrinolysis?

Thomas C. Abshire, Stuart H. Gold, Lorrie F. Odom, Steven D Carson, William E. Hathaway

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Little information is available on the prevalence and etiology of the coagulopathy present in some children with acute leukemia at disease presentation. We studied 102 children with newly diagnosed acute leukemia (50 retrospective: Group A; and 52 prospective: Group B) with prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), fibrinogen (FIB), and fibrin degradation products (FDP). All patients in Group B also had assessment of thrombin activation by measurement of the crosslinked fibrin fragment, D‐dimer, and of primary fibrinolysis with the Bβ 1‐42 peptide. Additionally, ten patients from Group B had Factors II, V, VII, and × measured, and eight of these patients had measurement of tissue factor from sonicated bone marrow cells. Thirty‐two percent of Group A and 40% of Group B had totally normal coagulation studies, whereas 20% of Group A and 10% of Group B had a severe coagulopathy on disease presentation. A high percentage of both groups had elevated PT (Group A, 52%; Group B, 27%) and increased FDP (Group A, 39%; Group B, 25%). In Group B, 38% of the patients had a positive D‐dimer, whereas only 4% of this prospective group had an elevated Bβ 1‐42 peptide (P < 0.00001). Nine of ten patients with a positive D‐dimer had low levels of one or more of the extrinsic pathway factors. Three of four patients with the highest tissue factor levels were of monocytoid leukemia cell type. These data indicate that the coagulopathy associated with acute leukemia of childhood is usually mediated by thrombin activation.

Original languageEnglish (US)
Pages (from-to)716-721
Number of pages6
JournalCancer
Volume66
Issue number4
DOIs
StatePublished - Jan 1 1990

Fingerprint

Fibrinolysis
Thrombin
Leukemia
Fibrin Fibrinogen Degradation Products
Prothrombin Time
Thromboplastin
Thrombin Time
Partial Thromboplastin Time
Prothrombin
Fibrin
Bone Marrow Cells

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

The coagulopathy of childhood leukemia thrombin activation or primary fibrinolysis? / Abshire, Thomas C.; Gold, Stuart H.; Odom, Lorrie F.; Carson, Steven D; Hathaway, William E.

In: Cancer, Vol. 66, No. 4, 01.01.1990, p. 716-721.

Research output: Contribution to journalArticle

Abshire, Thomas C. ; Gold, Stuart H. ; Odom, Lorrie F. ; Carson, Steven D ; Hathaway, William E. / The coagulopathy of childhood leukemia thrombin activation or primary fibrinolysis?. In: Cancer. 1990 ; Vol. 66, No. 4. pp. 716-721.
@article{8efe047eafe441e29cf53dae11f77cc5,
title = "The coagulopathy of childhood leukemia thrombin activation or primary fibrinolysis?",
abstract = "Little information is available on the prevalence and etiology of the coagulopathy present in some children with acute leukemia at disease presentation. We studied 102 children with newly diagnosed acute leukemia (50 retrospective: Group A; and 52 prospective: Group B) with prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), fibrinogen (FIB), and fibrin degradation products (FDP). All patients in Group B also had assessment of thrombin activation by measurement of the crosslinked fibrin fragment, D‐dimer, and of primary fibrinolysis with the Bβ 1‐42 peptide. Additionally, ten patients from Group B had Factors II, V, VII, and × measured, and eight of these patients had measurement of tissue factor from sonicated bone marrow cells. Thirty‐two percent of Group A and 40{\%} of Group B had totally normal coagulation studies, whereas 20{\%} of Group A and 10{\%} of Group B had a severe coagulopathy on disease presentation. A high percentage of both groups had elevated PT (Group A, 52{\%}; Group B, 27{\%}) and increased FDP (Group A, 39{\%}; Group B, 25{\%}). In Group B, 38{\%} of the patients had a positive D‐dimer, whereas only 4{\%} of this prospective group had an elevated Bβ 1‐42 peptide (P < 0.00001). Nine of ten patients with a positive D‐dimer had low levels of one or more of the extrinsic pathway factors. Three of four patients with the highest tissue factor levels were of monocytoid leukemia cell type. These data indicate that the coagulopathy associated with acute leukemia of childhood is usually mediated by thrombin activation.",
author = "Abshire, {Thomas C.} and Gold, {Stuart H.} and Odom, {Lorrie F.} and Carson, {Steven D} and Hathaway, {William E.}",
year = "1990",
month = "1",
day = "1",
doi = "10.1002/1097-0142(19900815)66:4<716::AID-CNCR2820660420>3.0.CO;2-B",
language = "English (US)",
volume = "66",
pages = "716--721",
journal = "Cancer",
issn = "0008-543X",
publisher = "John Wiley and Sons Inc.",
number = "4",

}

TY - JOUR

T1 - The coagulopathy of childhood leukemia thrombin activation or primary fibrinolysis?

AU - Abshire, Thomas C.

AU - Gold, Stuart H.

AU - Odom, Lorrie F.

AU - Carson, Steven D

AU - Hathaway, William E.

PY - 1990/1/1

Y1 - 1990/1/1

N2 - Little information is available on the prevalence and etiology of the coagulopathy present in some children with acute leukemia at disease presentation. We studied 102 children with newly diagnosed acute leukemia (50 retrospective: Group A; and 52 prospective: Group B) with prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), fibrinogen (FIB), and fibrin degradation products (FDP). All patients in Group B also had assessment of thrombin activation by measurement of the crosslinked fibrin fragment, D‐dimer, and of primary fibrinolysis with the Bβ 1‐42 peptide. Additionally, ten patients from Group B had Factors II, V, VII, and × measured, and eight of these patients had measurement of tissue factor from sonicated bone marrow cells. Thirty‐two percent of Group A and 40% of Group B had totally normal coagulation studies, whereas 20% of Group A and 10% of Group B had a severe coagulopathy on disease presentation. A high percentage of both groups had elevated PT (Group A, 52%; Group B, 27%) and increased FDP (Group A, 39%; Group B, 25%). In Group B, 38% of the patients had a positive D‐dimer, whereas only 4% of this prospective group had an elevated Bβ 1‐42 peptide (P < 0.00001). Nine of ten patients with a positive D‐dimer had low levels of one or more of the extrinsic pathway factors. Three of four patients with the highest tissue factor levels were of monocytoid leukemia cell type. These data indicate that the coagulopathy associated with acute leukemia of childhood is usually mediated by thrombin activation.

AB - Little information is available on the prevalence and etiology of the coagulopathy present in some children with acute leukemia at disease presentation. We studied 102 children with newly diagnosed acute leukemia (50 retrospective: Group A; and 52 prospective: Group B) with prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), fibrinogen (FIB), and fibrin degradation products (FDP). All patients in Group B also had assessment of thrombin activation by measurement of the crosslinked fibrin fragment, D‐dimer, and of primary fibrinolysis with the Bβ 1‐42 peptide. Additionally, ten patients from Group B had Factors II, V, VII, and × measured, and eight of these patients had measurement of tissue factor from sonicated bone marrow cells. Thirty‐two percent of Group A and 40% of Group B had totally normal coagulation studies, whereas 20% of Group A and 10% of Group B had a severe coagulopathy on disease presentation. A high percentage of both groups had elevated PT (Group A, 52%; Group B, 27%) and increased FDP (Group A, 39%; Group B, 25%). In Group B, 38% of the patients had a positive D‐dimer, whereas only 4% of this prospective group had an elevated Bβ 1‐42 peptide (P < 0.00001). Nine of ten patients with a positive D‐dimer had low levels of one or more of the extrinsic pathway factors. Three of four patients with the highest tissue factor levels were of monocytoid leukemia cell type. These data indicate that the coagulopathy associated with acute leukemia of childhood is usually mediated by thrombin activation.

UR - http://www.scopus.com/inward/record.url?scp=0025003474&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025003474&partnerID=8YFLogxK

U2 - 10.1002/1097-0142(19900815)66:4<716::AID-CNCR2820660420>3.0.CO;2-B

DO - 10.1002/1097-0142(19900815)66:4<716::AID-CNCR2820660420>3.0.CO;2-B

M3 - Article

VL - 66

SP - 716

EP - 721

JO - Cancer

JF - Cancer

SN - 0008-543X

IS - 4

ER -