In vitro monitoring of endothelial complications following hematopoietic allogeneic stem cell transplantation

Ganster, A.; Brucker, I.; Holler, Ernst; Hahn, J.; Bremm, Heike; Andreesen, Reinhard; Eissner, Guenther

doi:10.1038/sj.bmt.1704354

Cited by 7 publications

(4 citation statements)

References 11 publications

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“…Serum levels of VCAM-1 within the first 100 days also correlated with GVHD. 38 Our group, in collaboration with the Regensburg group, examined the effect of the different types of HSCT and the conditioning regimens applied on the integrity of the endothelium through a series of in vitro studies. 15,30 We applied a laboratory-based macrovascular cell model to explore more deeply the effect of the soluble plasma factors released during HSCT on resting ECs.…”

Section: Cecs and Microparticlesmentioning

confidence: 99%

The role of the endothelium in the short-term complications of hematopoietic SCT

Carreras

Díaz‐Ricart

2011

Bone Marrow Transplant

248

246

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Section: Cecs and Microparticlesmentioning

confidence: 99%

The role of the endothelium in the short-term complications of hematopoietic SCT

Carreras

Díaz‐Ricart

2011

Bone Marrow Transplant

248

246

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“…Decrements in platelet numbers are not associated with an enhanced fibrinolytic response as would be expected. This finding may be explained with the impairment of the vascular profibrinolytic pool following HSCT-induced vascular injury [43].…”

Section: Discussionmentioning

confidence: 98%

Unchanged global fibrinolytic capacity during the course of hematopoietic stem cell transplantation

Aksu

Beyazıt²,

Haznedaroğlu³

et al. 2006

Blood Coagulation &Amp; Fibrinolysis

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Hemostatic changes due to vascular endothelial damage are seen during the course of hematopoietic stem cell transplantation (HSCT). The fibrinolytic response to ongoing hemostatic activation in HSCT remains to be elucidated. Global fibrinolytic capacity (GFC) is a novel method, which reflects the amount of generated D-dimer when fibrinolysis of a freeze-dried fibrin clot is stopped by introducing aprotinin. GFC is sensitive to all the factors involved in the process of fibrinolysis. The aim of this study was to serially assess GFC at certain critical time points (days -1, +7, +14, +21 prior to and following stem cell infusion) during the course of HSCT. The study group comprised 16 patients with hematological malignancies (11 women, five men; median age 32+/-9 years) in whom HSCT had been performed. Thirty healthy adults (21 women, nine men; median age 31+/-7 years) served as controls. In this study, global fibrinolytic response, as reflected by GFC, was unchanged despite ongoing hemostatic activation, as indicated by D-dimer, moreover GFC remained stable, despite the development of thrombocytopenia associated with HSCT prior to platelet engraftment. Our results indicate that a global fibrinolytic response was impaired as a compensatory response to endothelial activation and to other hemostatic changes seen in HSCT. Further studies in larger HSCT populations are warranted to better understand the implications of these findings.

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“…In the auto-HCT, both engraftment [ 37 ] and the use of G-CSF could act as the triggers of the damage seen when ECs were grown in the presence of patients sera obtained at day +14. In the allo-HCT, the alloreactivity could explain the increase in the levels of damage biomarkers in response to sera collected at day +21 [ 38 , 39 ]. These results may be the consequence of the effect on the endothelium of the conditioning treatment, the administration of pro-inflammatory (G-CSF) or immunomodulatory agents, and the onset of donor leukocyte engraftment.…”

Section: Hct Is Associated With Endothelial Dysfunction Even In the Absence Of Any Related Complicationmentioning

confidence: 99%

Endothelial Dysfunction in Hematopoietic Cell Transplantation

Palomo¹,

Díaz‐Ricart²,

Carreras³

2019

CHI

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The goal of this review is to look at the role of endothelial damage and dysfunction in the initiation and development of early complications that appear after hematopoietic cell transplantation (HCT). These early complications share overlapping clinical manifestations and the suspicion of underlying endothelial damage. Several studies using different approaches, such as animal and in vitro models, the analysis of soluble biomarkers and clinical findings have provided evidence of this endothelial dysfunction. Historically, the first complication in which the role of endothelial damage was elucidated was the veno-oclusive disease/sinusoidal obstructive syndrome. In the last two decades, increasing evidence of the implication of the endothelium in the pathophysiology of other syndromes such as capillary leak syndrome, transplant-associated microangiopathy, or even graft versus host disease has accumulated. This knowledge opens up potential pharmacologic interventions to prevent/and/or treat endothelial damage and, therefore, to improve the outcome of patients receiving HCT.

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In vitro monitoring of endothelial complications following hematopoietic allogeneic stem cell transplantation

Cited by 7 publications

References 11 publications

The role of the endothelium in the short-term complications of hematopoietic SCT

The role of the endothelium in the short-term complications of hematopoietic SCT

Unchanged global fibrinolytic capacity during the course of hematopoietic stem cell transplantation

Endothelial Dysfunction in Hematopoietic Cell Transplantation

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