International Journal of Critical Illness and Injury Science

: 2015  |  Volume : 5  |  Issue : 4  |  Page : 230--231

Does erythropoietin reactivate bone marrow dysfunction in trauma hemorrhagic shock?

Manoj Kumar, Sanjeev Bhoi 
 Department of Emergency Medicine, Jai Prakash Narayan Apex Trauma Center, All Institute of Medical Sciences, New Delhi, India

Correspondence Address:
Sanjeev Bhoi
Emergency Medicine, Jai Prakash Narayan Apex Trauma Center, All India Institute of Medical Sciences, New Delhi - 110 022

How to cite this article:
Kumar M, Bhoi S. Does erythropoietin reactivate bone marrow dysfunction in trauma hemorrhagic shock?.Int J Crit Illn Inj Sci 2015;5:230-231

How to cite this URL:
Kumar M, Bhoi S. Does erythropoietin reactivate bone marrow dysfunction in trauma hemorrhagic shock?. Int J Crit Illn Inj Sci [serial online] 2015 [cited 2022 Jul 3 ];5:230-231
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Full Text

Hemorrhagic shock (HS) and its sequelae of multiorgan dysfunction (MOD) and sepsis are the major leading cause of death after trauma.[1] Fluid, blood and its component, and stopping of bleeders have been the cornerstone of management since many decades. Cytokine storm dysregulates balance of pro-inflammatory and anti-inflammatory cytokines, which leads to clinically fatal outcome.[2] The role of bone marrow (BM) in trauma hemorrhagic shock (T/HS) has been ill-understood. BM dysfunction in T/HS leads to persistent anemia with increased susceptibility to infection and sepsis, mainly due to dyserythropoiesis and myelopoesis.BM dysfunction is a multifactorial process. Excessive pro-inflammatory cytokine milieu and elevated levels of circulating catecholamines change the behavior BM microenvironment in a T/HS.[3],[4]

Survival and death machinery of hematopoietic stem and progenitor cells (HSPCs) is controlled by a complex interplay between intrinsic signals and stimuli from the surrounding BM microenvironment, inducing a dynamically balanced network of pro-survival and anti-survival influences. Alteration of this balance can lead to hematopoietic disorders, such as myeloproliferative disorders and BM dysfunction.[5]

Human and animal model have shown that erythropoietin (EPO) acts as an anti-apoptotic, neuroprotective, anti-inflammatory, angiogenesis and stabilization of neurovascular function, and reduces oxidative stress by stimulating cell survival pathway (PI3k/Akt pathway). Treatment of rats with EPO for 3 days prior to induction of T/HS significantly attenuated renal (glomerular) dysfunction, liver and neuromuscular injury compared with pretreatment with vehicle.[6],[7] In humans, EPO (4,000 IU) injection into the site of tibiofibular fractures may possibly accelerate healing.[8]

EPO receptor are found onearly burst forming unit-erythroid (BFU-E), as well as late erythroid progenitor cells (colony forming unit-erythroid (CFU-E), the first cells recognizable as committed to erythroid differentiation and nonhematopoietic tissue including central nervous system, endothelium, cardiac myocytes, kidney, and some solid cancer line.[7],[8] Livingston et al., studied behavior of peripheral and BM hematopoietic progenitor cell growth (HPCs) at various time intervals. Suppressed HPCs'growths were observed without reactivation.[3]

The author feels that in-vitro BM function may be reactivated with EPO and growth factors. Synergistic or additive effect of growth factors (EPO, interleukin-3 (IL-3), and granulocyte-macrophage colony-stimulating factor (GM-CSF) on HPCs' growth in T/HS can be studied. It may provide insight to the effect of EPO with or without growth factors (IL3 and GM-CSF) on duration of recovery time of suppressed hematopoietic progenitor cell lines. This may provide the hypothesis in future human trial on use of growth factors in T/HS.


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