Endocrine Abstracts

At patients with premature ovarian failure, follicular endowment is very low and therefore is deficient ovarian hormonogenesis. As the number of follicles is lower, the lifetime of the ovary is reduced, representing a clinical spectrum from total or partial absence of pubertal sexualisation by early onset climacteric. The disruption of ovarian hormones that control bone homeostasis, is disturb-training report bone resorption with decreased bone mass and osteoporosis.

Method: The study was conducted on 48 patients whose age ranged between 20–38 years. Investigations were focused on the study hormonology FSH, LH, PRL, oestradiol, progesterone. Pelvic ultrasound was also performed utero-ovarian. At all patients the bone mineral density (BMD) was assessed by dual X-ray absorptiometry (DEXA). As biochemical markers of bone turnover were studied and serum Osteocalcine CrossLaps by ELISA.

Results: Hormonal dosages showed low levels of oestradiol and progesterone, but those of gonadotrophic hormones (LH, FSH) were between 210–385 mil/ml (upper limit of normal: 0.110 to 190 mil/ml). BMD measurement showed the presence of osteoporosis in 22 cases, representing 45.8% of all cases investigated. BMD is correlated with biochemical markers of bone turnover.

Conclusion: i) A study of BMD and biochemical markers of bone turnover in premature ovarian failure, it must be conducted regularly to identify patients who rapidly lose bone mass and increased risk of osteoporosis.

ii) The estrogen-progestive substitution represents the therapeutic attitude which is the first choice for premature ovarian failure to prevent osteoporosis, and metabolic complications of visceral.

iii) Patients with osteoporosis will be associated the antiresorbtion or proformation medication to prevent fragility fractures.