ABSTRACT
Numerous systemic diseases alter gonadal function in males, either by inhibiting testosterone synthesis in the testes or by altering the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary. Severe systemic illness results in the marked inhibition of LH and FSH release, thereby causing subsequent hypotestosteronemia (1-5). LH pulsatility is likewise decreased during critical illness (6). Administration of dopamine during the period of critical illness further decreases gonadotropin secretion (7). Table 1 summarizes the changes in the hypothalamic-pituitarytesticular axis that occur in a variety of chronic diseases. Unfortunately, these are limited studies that examine the effect of testosterone replacement in disease states, making it nearly impossible to conclude whether or not the testosterone decrease observed in disease processes is protective or harmful.
