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Review
. 2024 Apr;99 Suppl 1(Suppl 1):S28-S35.
doi: 10.1002/ajh.27296. Epub 2024 Apr 3.

Sex dimorphisms in coagulation: Implications in trauma-induced coagulopathy and trauma resuscitation

Affiliations
Review

Sex dimorphisms in coagulation: Implications in trauma-induced coagulopathy and trauma resuscitation

Julia R Coleman et al. Am J Hematol. 2024 Apr.

Abstract

Trauma-induced coagulopathy (TIC) is one of the leading causes of preventable death in injured patients. Consequently, it is imperative to understand the mechanisms underlying TIC and how to mitigate this mortality. An opportunity for advancement stems from the awareness that coagulation demonstrates a strong sex-dependent effect. Females exhibit a relative hypercoagulability compared to males, which persists after injury and confers improved outcomes. The mechanisms underlying sex dimorphisms in coagulation and its protective effect after injury have yet to be elucidated. This review explores sex dimorphisms in enzymatic hemostasis, fibrinogen, platelets, and fibrinolysis, with implications for resuscitation of patients with TIC.

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Conflict of interest statement

Conflict of interest: The authors have no conflicts of interest to report.

Figures

Figure 1.
Figure 1.
Overlapping representative thrombelastography tracings of males and females, demonstrating the multi-faceted hypercoagulability of females.
Figure 2.
Figure 2.
Estrogen release after injury mitigates the pathologic immune, coagulation, and physiologic response to trauma.
Figure 3.
Figure 3.
Female sex is associated with increased coagulation factors and thrombin promoters (green) and decreased thrombin inhibitors (red), resulting in net increased thrombin generation in females.
Figure 4.
Figure 4.
Female platelets demonstrate increased functional activity and resistance to inhibition as compared to male platelets.
Figure 5.
Figure 5.
Salient features of female-specific hypercoagulability.

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