Bone loss during gonadotropin-releasing hormone agonist treatment in girls with true precocious puberty is not due to an impairment of calcitonin secretion.

Gonadal steroids drive the significant bone mineral increase that occurs at puberty, while estrogen deprivation in postmenopausal women results in bone mass reduction. We looked for bone mineralization in girls with true precocious puberty (TPP) before and after six months of LH-RH analogs treatment. Calcitonin secretion in these girls were studied too. Bone mineral content (BMC) and BMC/BW ratio (single photon absorptiometry) were measured in seven girls (aged 4.3 to 8.7 years) with TPP before LH-RH agonist therapy (long acting D-Trp6-LH-RH 60 micrograms/kg im every 28 days) was started; the patients were reevaluated after six months of therapy. Before therapy, BMC and BMC/BW were increased for chronological age but appropriate for bone age according to our mineralization normative data. After six months of LH-RH analog administration, 17 beta-estradiol and LH levels were suppressed and BMC and BMC/BW showed a small but significant decrease (respectively -5.4%, p less than 0.02 and -6.3%, p less than 0.02). Basal and calcium stimulated calcitonin levels (total and extractable) did not significantly change during the study period. We conclude that in girls with TPP bone mineralization was increased for chronological age but normal for bone age. The estrogen withdrawal secondary to LH-RH analog therapy caused a reduction in bone mass. Such a bone loss is not due to an impairment of calcitonin secretion.