Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease

Eduard J. van Beers; Marianne C. L. Schaap; Rene J. Berckmans; Rienk Nieuwland; Augueste Sturk; Frederiek F. van Doormaal; Joost C. M. Meijers; Bart J. Biemond

doi:10.3324/haematol.2009.008938

Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease

Eduard J. van Beers, Marianne C. L. Schaap, Rene J. Berckmans, Rienk Nieuwland, Augueste Sturk, Frederiek F. van Doormaal, Joost C. M. Meijers, Bart J. Biemond^*,

^*Corresponding author for this work

Hematology/Van Creveldclinic

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

Background

Sickle cell disease is characterized by a hypercoagulable state as a result of multiple factors, including chronic hemolysis and circulating cell-derived microparticles. There is still no consensus on the cellular origin of such microparticles and the exact mechanism by which they may enhance coagulation activation in sickle cell disease.

Design and Methods

In the present study, we analyzed the origin of circulating microparticles and their procoagulant phenotype during painful crises and steady state in 25 consecutive patients with sickle cell disease.

Results

The majority of microparticles originated from platelets (GPIIIa,CD61) and erythrocytes (glycophorin A,CD235), and their numbers did not differ significantly between crisis and steady state. Erythrocyte-derived microparticles strongly correlated with plasma levels of markers of hemolysis, i.e. hemoglobin (r=-0.58, p0.05). The extent of factor XI inhibition was associated with erythrocyte-derived microparticles (r=0.50, p=0.023).

Conclusions

We conclude that the procoagulant state in sickle cell disease is partially explained by the factor XI-dependent procoagulant properties of circulating erythrocyte-derived microparticles.

Original language	English
Pages (from-to)	1513-1519
Number of pages	7
Journal	Haematologica
Volume	94
Issue number	11
DOIs	https://doi.org/10.3324/haematol.2009.008938
Publication status	Published - Nov 2009

Keywords

microparticles
sickle cell disease
coagulation activation
hemolysis
PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA
SUPPORT COAGULATION
PLATELET ACTIVATION
THROMBIN GENERATION
PROCOAGULANT
THALASSEMIA
SPICULES
SEPSIS

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10.3324/haematol.2009.008938

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@article{25b92c6fa918473faeb542f0e44bec7a,

title = "Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease",

abstract = "BackgroundSickle cell disease is characterized by a hypercoagulable state as a result of multiple factors, including chronic hemolysis and circulating cell-derived microparticles. There is still no consensus on the cellular origin of such microparticles and the exact mechanism by which they may enhance coagulation activation in sickle cell disease.Design and MethodsIn the present study, we analyzed the origin of circulating microparticles and their procoagulant phenotype during painful crises and steady state in 25 consecutive patients with sickle cell disease.ResultsThe majority of microparticles originated from platelets (GPIIIa,CD61) and erythrocytes (glycophorin A,CD235), and their numbers did not differ significantly between crisis and steady state. Erythrocyte-derived microparticles strongly correlated with plasma levels of markers of hemolysis, i.e. hemoglobin (r=-0.58, p0.05). The extent of factor XI inhibition was associated with erythrocyte-derived microparticles (r=0.50, p=0.023).ConclusionsWe conclude that the procoagulant state in sickle cell disease is partially explained by the factor XI-dependent procoagulant properties of circulating erythrocyte-derived microparticles.",

keywords = "microparticles, sickle cell disease, coagulation activation, hemolysis, PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA, SUPPORT COAGULATION, PLATELET ACTIVATION, THROMBIN GENERATION, PROCOAGULANT, THALASSEMIA, SPICULES, SEPSIS",

author = "\{van Beers\}, \{Eduard J.\} and Schaap, \{Marianne C. L.\} and Berckmans, \{Rene J.\} and Rienk Nieuwland and Augueste Sturk and \{van Doormaal\}, \{Frederiek F.\} and Meijers, \{Joost C. M.\} and Biemond, \{Bart J.\}",

year = "2009",

month = nov,

doi = "10.3324/haematol.2009.008938",

language = "English",

volume = "94",

pages = "1513--1519",

journal = "Haematologica",

issn = "0390-6078",

publisher = "Ferrata Storti Foundation",

number = "11",

}

TY - JOUR

T1 - Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease

AU - van Beers, Eduard J.

AU - Schaap, Marianne C. L.

AU - Berckmans, Rene J.

AU - Nieuwland, Rienk

AU - Sturk, Augueste

AU - van Doormaal, Frederiek F.

AU - Meijers, Joost C. M.

AU - Biemond, Bart J.

PY - 2009/11

Y1 - 2009/11

N2 - BackgroundSickle cell disease is characterized by a hypercoagulable state as a result of multiple factors, including chronic hemolysis and circulating cell-derived microparticles. There is still no consensus on the cellular origin of such microparticles and the exact mechanism by which they may enhance coagulation activation in sickle cell disease.Design and MethodsIn the present study, we analyzed the origin of circulating microparticles and their procoagulant phenotype during painful crises and steady state in 25 consecutive patients with sickle cell disease.ResultsThe majority of microparticles originated from platelets (GPIIIa,CD61) and erythrocytes (glycophorin A,CD235), and their numbers did not differ significantly between crisis and steady state. Erythrocyte-derived microparticles strongly correlated with plasma levels of markers of hemolysis, i.e. hemoglobin (r=-0.58, p0.05). The extent of factor XI inhibition was associated with erythrocyte-derived microparticles (r=0.50, p=0.023).ConclusionsWe conclude that the procoagulant state in sickle cell disease is partially explained by the factor XI-dependent procoagulant properties of circulating erythrocyte-derived microparticles.

AB - BackgroundSickle cell disease is characterized by a hypercoagulable state as a result of multiple factors, including chronic hemolysis and circulating cell-derived microparticles. There is still no consensus on the cellular origin of such microparticles and the exact mechanism by which they may enhance coagulation activation in sickle cell disease.Design and MethodsIn the present study, we analyzed the origin of circulating microparticles and their procoagulant phenotype during painful crises and steady state in 25 consecutive patients with sickle cell disease.ResultsThe majority of microparticles originated from platelets (GPIIIa,CD61) and erythrocytes (glycophorin A,CD235), and their numbers did not differ significantly between crisis and steady state. Erythrocyte-derived microparticles strongly correlated with plasma levels of markers of hemolysis, i.e. hemoglobin (r=-0.58, p0.05). The extent of factor XI inhibition was associated with erythrocyte-derived microparticles (r=0.50, p=0.023).ConclusionsWe conclude that the procoagulant state in sickle cell disease is partially explained by the factor XI-dependent procoagulant properties of circulating erythrocyte-derived microparticles.

KW - microparticles

KW - sickle cell disease

KW - coagulation activation

KW - hemolysis

KW - PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA

KW - SUPPORT COAGULATION

KW - PLATELET ACTIVATION

KW - THROMBIN GENERATION

KW - PROCOAGULANT

KW - THALASSEMIA

KW - SPICULES

KW - SEPSIS

U2 - 10.3324/haematol.2009.008938

DO - 10.3324/haematol.2009.008938

M3 - Article

C2 - 19815831

SN - 0390-6078

VL - 94

SP - 1513

EP - 1519

JO - Haematologica

JF - Haematologica

IS - 11

ER -

Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease

Abstract

Keywords

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