Luteinizing hormonetestosterone axis

The low serum testosterone concentrations despite elevated luteinizing hormone (LH) levels documented during the acute stress of surgery or myocardial infarction suggest an immediate stress-induced Leydig cell suppression (Wang et al 1978a,b, Dong et al 1992), the exact cause of which remains obscure. A role for inflammatory cytokines (IL1 and IL2) is possible, as suggested by experimental studies. It may be considered appropriate that the secretion of anabolic androgens be switched off in circumstances of acute stress, in order to reduce the consumption of energy and substrates at such a critical life-threatening time.

As critical illness becomes prolonged, hypogonadotropic hypogonadism ensues (Vogel et al 1985, Woolf et al 1985). Circulating levels of testosterone become extremely low, often undetectable in men whereas oestradiol concentrations are reduced to a lesser degree, thereby increasing the oestradiol:testosterone molar ratio. The progressive decline in serum gonadotropin levels, however, appears to lag behind the rapid decline in serum testosterone. In men with PCI, a high LH pulse frequency with an abnormally low LH pulse amplitude is seen and this has been interpreted as an impaired LH response to very low circulating testosterone levels (Van den Berghe et al 1994b). Endogenous dopamine, opiates IL1, and the 'relatively spared' oestradiol level may be involved in the pathogenesis of the gonadotropin deficiency. Androgen treatment in men affected by prolonged critical illness failed to induce conclusive clinical benefit (Tweedle et al 1972). An alternative approach with exogenous gonadotropin-releasing hormone (GnRH) has proved a little more promising in that the gonadotropin deficiency could be partially reversed with pulsatile GnRH administered intravenously (Van den Berghe et al 2001). The inability to completely reverse the profound hypogonadotropic hypogonadal state may be due to relative pituitary desensitization to GnRH or enhanced-feedback inhibition from the markedly elevated oestradiol:testosterone molar ratio. Peripheral tissues were sensitive to transient changes in sex steroids, as reflected by anabolic and inflammatory responses (Van den Berghe et al 2001).

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