|Year : 2016 | Volume
| Issue : 2 | Page : 53
What's new in critical illness and injury science? estrogen: Is it a new therapeutic paradigm for trauma-hemorrhagic shock?
Sanjeev Bhoi, Shreshtha Tiwari, Manoj Kumar
Department of Emergency Medicine, Jai Prakash Narayan Apex Trauma Centre, All Institute of Medical Sciences, New Delhi, India
|Date of Web Publication||26-May-2016|
Department of Emergency Medicine, Jai Prakash Narayan Apex Trauma Centre, All India Institute of Medical Sciences, New Delhi - 110 029
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Bhoi S, Tiwari S, Kumar M. What's new in critical illness and injury science? estrogen: Is it a new therapeutic paradigm for trauma-hemorrhagic shock?. Int J Crit Illn Inj Sci 2016;6:53
|How to cite this URL:|
Bhoi S, Tiwari S, Kumar M. What's new in critical illness and injury science? estrogen: Is it a new therapeutic paradigm for trauma-hemorrhagic shock?. Int J Crit Illn Inj Sci [serial online] 2016 [cited 2022 Jan 18];6:53. Available from: https://www.ijciis.org/text.asp?2016/6/2/53/183021
Hemorrhagic shock (HS) is the most common cause of death after trauma. Mortality due to HS is about 50%. Therapeutic uses of drugs as adjuncts are limited. Fluid, blood component, and control of hemorrhage have been the cornerstone of management. Resuscitation with fluids and blood products induces reperfusion ischemia due to the production of reactive oxygen species and activation of immune cells.
Cytokine storm dysregulates balance of pro- and anti-inflammatory cytokines, which leads to suppression of immune system. Raju et al. reported suppression of immune system is characterized by decreased T- and B-cell function. The function of splenic dendritic cells and macrophage antigen presenting function were depressed following trauma-hemorrhage (TH).
Immunological alteration or its complication following T/HS may be reversed by estrogen administration. In addition, suppressed cardiac, hepatocellular, and immune functions were maintained with estrogen treatment in male mice, rats, and proestrus females following TH., Raju et al. reported that female tolerate trauma and sepsis stimuli than male and that estrogen has a protective effect. Li et al. showed treatment with estrogen increased vascular reactivity and responsiveness in both male and female rats of 8–24 week. Protective effects of estrogen were associated with G protein-coupled receptor 30, estrogen receptor-mediated Rho kinase, and protein kinase C pathway activation.
Sex dichotomies were observed in 7560 males and 2774 females from a large trauma registry. It showed that female sex protects from organ failure and sepsis after major TH.
Conjugated intravenous estrogen is used as a therapeutic option for massive dysfunctional uterine bleeding but its role in T/HS has not been defined. Future studies on humans may explore the therapeutic role of estrogen as an adjunct in patients presenting with trauma HS.
| References|| |
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