Many authors have shown that osteoporosis is an important complication in male hypogonadism, due to the chronic lack of androgens; but in hypogonadal males the pathogenesis of osteopenia isn't completely explained. In this work we examined in 10 hypogonadal males (4 with Klinefelter's Syndrome and 6 with Hypogonadotropic Hypogonadism) lumbar bone mineral content (BMC) and the effects of testosterone (Sustanon) administration on BMC and other phosphocalcium parameters. We evidenced lower BMC levels in hypogonadal subjects if compared to those observed in the control age-matched group; moreover after 3 months of treatment a statistically significant increment of plasma bone gla protein, calcitonin and lumbar BMC was observed. On the contrary no significant variation was observed in osteoclastic indexes (PTH-MM, OHPU/CrU, CaU/CrU) after treatment. In addition both calcitonin basal levels and secretory reserve, measured with calcium infusion, were significantly increased after treatment. Our data confirm the hypothesis that androgen acts on bone principally directly at osteoblastic level, in a stimulatory manner, and indirectly, with calcitonin mediation, with inhibition of osteoclasts.
[Effect on phospho-calcium metabolism of testosterone administration in hypogonadal males]
ISAIA, Giovanni Carlo;
1990-01-01
Abstract
Many authors have shown that osteoporosis is an important complication in male hypogonadism, due to the chronic lack of androgens; but in hypogonadal males the pathogenesis of osteopenia isn't completely explained. In this work we examined in 10 hypogonadal males (4 with Klinefelter's Syndrome and 6 with Hypogonadotropic Hypogonadism) lumbar bone mineral content (BMC) and the effects of testosterone (Sustanon) administration on BMC and other phosphocalcium parameters. We evidenced lower BMC levels in hypogonadal subjects if compared to those observed in the control age-matched group; moreover after 3 months of treatment a statistically significant increment of plasma bone gla protein, calcitonin and lumbar BMC was observed. On the contrary no significant variation was observed in osteoclastic indexes (PTH-MM, OHPU/CrU, CaU/CrU) after treatment. In addition both calcitonin basal levels and secretory reserve, measured with calcium infusion, were significantly increased after treatment. Our data confirm the hypothesis that androgen acts on bone principally directly at osteoblastic level, in a stimulatory manner, and indirectly, with calcitonin mediation, with inhibition of osteoclasts.
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