BACKGROUNDBenign prostatic hyperplasia (BPH) develops in elderly males when serum androgens are relatively lower than in healthy younger males, but it is not well understood whether and how sex steroids are altered in prostatic hyperplasia. It is also uncertain whether there is any change in sex steroid levels in males older than 40 years of age. The use of androgens in elderly males is often discouraged because of the probable worsening effect of androgens on prostatism. This study aimed to determine the relationship between prostatic hyperplasia and sex steroid levels and whether there is any significant change in these hormones after the age of 40 years.SUBJECTS AND METHODSWe studied healthy males of age ≥40 years with (n=92) or without (n=93) clinical prostatic hyperplasia. Serum testosterone, estradiol, gonadotrophins and sex hormone-binding globulin (SHBG) were compared. The hormones and SHBG were also correlated with age.RESULTSNo significant difference was found in any hormone in cases with prostatic hyperplasia as compared with the controls. There was no significant age-related change in any hormone except estradiol where as a negative correlation (P<.003) with age was found.CONCLUSIONSSerum sex steroids and SHBG remained unchanged in symptomatic prostatic hyperplasia and except for estradiol there was no significant age-related change in serum testosterone, gonadotrophins and SHBG in healthy males after the fourth decade. More studies are needed to confirm the age-related decline of estrogens in males.

The role of endogenous opioids in the control of gonadotropin secretion in uremic male rats was investigated using the narcotic antagonist, naloxone. In order to eliminate the effect of weight loss due to uremia-induced anorexia as a cause of previously described altered gonadotropin secretion in uremia, we also studied a group of normal pair-fed control animals who exhibited a weight loss comparable to that of the uremic animals. Naloxone administration had no effect on the basal or LRH-stimulated peak concentrations of LH and FSH in the normal or the uremic rats. Basal and LRH-stimulated gonadotropin responses in the pair-fed rats were comparable to those seen in the normal rats. Similarly, opoid blockade produced no change in the basal or LRH-stimulated gonadotropin responses in the pair-fed animals. Testosterone concentrations were significantly lower in the uremic and pair-fed animals compared to the normal rats. The data suggest that experimental renal failure is not associated with altered opioidergic tone, as it relates to gonadotropin secretion, or to diminished sensitivity of the gonadotroph to LRH stimulation. The decreased testosterone concentration seen in the uremic and pair-fed rats may reflect abnormalities in gonadal hormone secretion due to primary pathology occurring at the level of the gonad. These abnormalities may be reflected as diminished Leydig cell sensitivity to LH. The inappropriately low concentrations of LH in the presence of low testosterone together with normal gonadotropin response to exogenous LRH also suggest an abnormal secretion of endogenous LRH. It is not clear whether this presumed abnormality in LRH secretion is a primary event or is related to decreased testosterone production by the testes in the uremic and pair-fed rats.