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Critical illness is associated with profound and prolonged hypoandrogenemia; Sertoli cell function is less affected. 225 In the acute phase, a rise in gonadotropin levels may suggest Leydig cell dysfunction, 217,222 but more prolonged illness is associated with gonadotropin suppression. 216 A decrease in LH pulse amplitude that is only partially overcome with exogenous pulsatile GnRH treatment, and the failure of testosterone levels to rise into the normal range are consistent with a combined central and testicular cause of the profound hypoandrogenism. 226,227 Furthermore, as estradiol levels are maintained, it is postulated that this negative feedback may contribute to reduced basal and GnRH-stimulated LH release. 217 Exogenous dopamine or opioid therapy further suppresses GnRH secretion. Although the decrease in serum testosterone has been inversely related to degree of illness 228 and severity of major burns, 219 whether it is predictive of mortality is uncertain. 223,225 A role for testosterone therapy has been studied to a limited degree in men who experience major burns. In small studies, oxandrolone has been shown to promote wound healing, 229 and short-term intramuscular testosterone has been shown to reduce muscle catabolism , 230 but no agreement has been reached as yet regarding the use of androgens in the management of severe illness and catabolic states. 231