Endocrine Abstracts

BACKGROUND: DHEA and DHEAS, can be converted into Androstenedione, T and DHT as well as oestrogens by peripheral tissues. In normal men the conversion rate of IV-infused radiolabelled DHEAS to T is only 0.7%. In hypogonadal men, this conversion rate may be increased. We hypothesise that a pharmacological dose of orally administered DHEA may be able to raise plasma T into the normal range in hypogonadal men. METHODS: Local Ethical Committee Approval was obtained. Two groups (n=5 each), of hypogonadal and eugonadal Caucasian males were recruited. The hypogonadal men were withdrawn from regular T replacement until low baseline levels were achieved. On day 0 each subject received placebo, followed by clatharate-DHEA 800mg daily on day 1 for 5 days. Blood samples were taken at minus 1, 0, 2, 4, 8, 12, 24 hours on days 0, 1, 5, and pre-dose on days 3 and 4. RESULTS: The data was analysed using non-parametric Mann-Whitney U and Wilcoxon Matched-Pairs Tests. The primary end points were plasma T, DHEAS, and E2. T levels peaked at t=2hrs to 28.1 nanomoles per litre (SEM 3.29) in the eugonadal, and 11.3 nanomoles per litre (SEM 3.75) in the hypogonadal group. There was a greater percentage rise in the hypogonadal group with a significant rise on days 1 and 5 compared to baseline (Z=3.75, p<0.001, two-tailed). There was a highly significant rise in DHEAS and E2 levels in both groups on days 1 and 5 (p<0.001). E2 levels peaked at t=2 and t=4hrs. CONCLUSION: Administration of clatharate-DHEA 800mg daily results in a transient rise in T levels at 2 hours post dose. The absolute T values are within the physiological range and are lower in the hypogonadal group. Oral clatharate-DHEA is not suitable as replacement therapy in male hypogonadism.