Endothelial Dysfunction in Hematopoietic Cell Transplantation

Palomo, Marta; Díaz‐Ricart, Maribel; Carreras, Enric

doi:10.2991/chi.d.190317.001

Cited by 24 publications

(17 citation statements)

References 76 publications

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“…Biomarkers could be either: (a) diagnostic biomarker (that identifies patients at the onset of clinical disease); (b) prognostic (that identifies the likelihood of a clinical event occurrence in HCT recipients), or (c) predictive (that categorizes patients by their likelihood of response to a particular treatment when measured prior to the treatment) [ 2 ]. Since GVHD and RRTs share a common trigger, particularly damaged endothelium [ 5 ], circulating endothelial cells (CECs) have been evaluated as a diagnostic biomarker for SOS [ 6 ] and as a prognostic marker for endothelial damage [ 7 – 10 ], acute GVHD [ 7 , 11 ], and thrombotic microangiopathy (TMA) [ 12 ]. Similarly, regulatory T cells (Tregs) [ 13 ], CD146 + T cells [ 14 ] and invariant natural killer T cells [ 15 ] have been evaluated as diagnostic/prognostic biomarkers for acute GVHD.…”

Section: Introductionmentioning

confidence: 99%

Prognostic plasma biomarkers of early complications and graft‐versus‐host disease in patients undergoing allogeneic hematopoietic stem cell transplantation

Balakrishnan

Illangeswaran

Rajamani

et al. 2020

eJHaem

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Early complications post hematopoietic stem cell transplantation (HSCT) such as sinusoidal obstruction syndrome (SOS) and graft versus host disease (GVHD) can be life threatening. Although several biomarkers have been identified to correlate with these complications and their response to treatment, these are yet to be used in clinical practice. Here, we evaluated circulating endothelial cells (CECs) (n = 26) and plasma biomarkers (ST2, REG3α, VCAM1, ICAM1, TIM3) (N = 210) at early time points, to determine their association with early complications post‐HSCT. Elevated CEC counts at the end of conditioning was associated with GVHD, indicating endothelial damage during HSCT. Plasma levels of REG3α, VCAM1, ICAM1, and TIM3 on day 14 (D14) and D14 ICAM1 and D28 ST2 were significantly higher in patients with SOS and aGVHD, respectively. Upon sub‐group analysis, D28 ST2, D14/D28 REG3α, and D14 ICAM1 levels were significantly higher in patients with gastrointestinal GVHD, while D28 ST2 was higher in those with skin/liver GVHD. High ST2 levels on D28 was significantly associated with non‐relapse mortality (NRM) and overall survival. Our results suggest that elevated ST2 levels on D28 could predict the likelihood of developing aGVHD and could influence NRM and OS.

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Section: Introductionmentioning

confidence: 99%

Prognostic plasma biomarkers of early complications and graft‐versus‐host disease in patients undergoing allogeneic hematopoietic stem cell transplantation

Balakrishnan

Illangeswaran

Rajamani

et al. 2020

eJHaem

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“…The endothelial damage in HCT is multifactorial and cumulative ( 54 , 55 ) due to the effect of the conditioning regimen, calcineurin inhibitors, infections, graft vs. host disease and processes inherent to HCT such as the engraftment syndrome, among others ( 56 – 59 ). This endothelial damage leads to a release of proinflammatory cytokines and procoagulant factors together with nitric oxide depletion and an increase in the expression of adhesion molecules at cell surface.…”

Section: Complement Endothelial Damage In Thrombotic Microangiopathiesmentioning

confidence: 99%

Complement Mediated Endothelial Damage in Thrombotic Microangiopathies

et al. 2022

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Thrombotic microangiopathies (TMA) constitute a group of different disorders that have a common underlying mechanism: the endothelial damage. These disorders may exhibit different mechanisms of endothelial injury depending on the pathological trigger. However, over the last decades, the potential role of the complement system (CS) has gained prominence in their pathogenesis. This is partly due to the great efficacy of complement-inhibitors in atypical hemolytic syndrome (aHUS), a TMA form where the primary defect is an alternative complement pathway dysregulation over endothelial cells (genetic and/or adquired). Complement involvement has also been demonstrated in other forms of TMA, such as thrombotic thrombocytopenic purpura (TTP) and in Shiga toxin-producing Escherichia coli hemolytic uremic syndrome (STEC-HUS), as well as in secondary TMAs, in which complement activation occurs in the context of other diseases. However, at present, there is scarce evidence about the efficacy of complement-targeted therapies in these entities. The relationship between complement dysregulation and endothelial damage as the main causes of TMA will be reviewed here. Moreover, the different clinical trials evaluating the use of complement-inhibitors for the treatment of patients suffering from different TMA-associated disorders are summarized, as a clear example of the entry into a new era of personalized medicine in its management.

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“…This damage occurs in the early post-HCT aplastic phase and is generally caused by conditioning regimen in presence of concurrent risk factors (e.g. prolonged immobilization, severe infections, high dose busulfan) ( 43 ). The “second hit” causes further endothelial injury and initiates platelet aggregation and thrombus formation in microvessels.…”

Section: Introductionmentioning

confidence: 99%

Biomarkers for Early Complications of Endothelial Origin After Allogeneic Hematopoietic Stem Cell Transplantation: Do They Have a Potential Clinical Role?

et al. 2021

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Endothelial cell (EC) dysfunction causes a number of early and life-threatening post hematopoietic stem cell transplant (HCT) complications that result in a rapid clinical decline. The main early complications are graft-vs.-host disease (GVHD), transplant associated thrombotic microangiopathy (TA-TMA), and sinusoidal obstruction syndrome (SOS). Post-HCT endothelial dysfunction occurs as a result of chemotherapy, infections, and allogeneic reactivity. Despite major advances in transplant immunology and improvements in supportive care medicine, these complications represent a major obstacle for successful HCT. In recent years, different biomarkers have been investigated for early detection of post-transplant endothelial cell dysfunction, but few have been validated. In this review we will define GVHD, TA-TMA and SOS, summarize the current data available in HCT biomarker research and identify promising biomarkers for detection and diagnosis of early HCT complications.

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Endothelial Dysfunction in Hematopoietic Cell Transplantation

Cited by 24 publications

References 76 publications

Prognostic plasma biomarkers of early complications and graft‐versus‐host disease in patients undergoing allogeneic hematopoietic stem cell transplantation

Prognostic plasma biomarkers of early complications and graft‐versus‐host disease in patients undergoing allogeneic hematopoietic stem cell transplantation

Complement Mediated Endothelial Damage in Thrombotic Microangiopathies

Biomarkers for Early Complications of Endothelial Origin After Allogeneic Hematopoietic Stem Cell Transplantation: Do They Have a Potential Clinical Role?

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