Dehydroepiandrosterone

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Abstract
SEVERAL STUDIES indicate that cell-mediated immune responses are markedly depressed in male patients following trauma and hemorrhagic shock, and that these changes persist for as long as 10 days after resuscitation.1,2 Moreover, these depressed immune responses have been associated with an increased susceptibility to and mortality due to subsequent sepsis.3,4 Recent studies have suggested that male sex steroid hormones play a significant role in producing immunodepression following trauma-induced hemorrhage (hereafter referred to as trauma-hemorrhage).4-6 Support for this assertion comes from studies that showed that depletion of testosterone by castration of male mice before trauma-hemorrhage prevents the depression of splenocyte immune functions.5 Alternatively, administration of a testosterone receptor antagonist, eg, flutamide, in normal male animals following trauma-hemorrhage restores the depressed immune responses and increases the survival rate of animals subjected to subsequent sepsis. In contrast to male mice, female mice in the proestrus state of the estrus cycle demonstrate enhanced immune responses following trauma-hemorrhage.7 Thus, it appears that elevated levels of female sex hormones, ie, prolactin and estrogen, in the proestrus state contribute to sexual dimorphism in the immune response following trauma-hemorrhage.8