Bone Abstracts

Background: Premature ovarian insufficiency (POI) may manifest as primary or secondary amenorrhoea, reflecting differences in timing and duration of hypo-oestrogenaemia. Oestrogen exposure during puberty is pivotal for the accrual of peak bone mineral density (BMD).

Aim: To assess whether exposure to endogenous oestrogen sufficient to achieve spontaneous menarche is associated with differences in BMD at first measurement in adolescents with POI.

Methods: Retrospective review of patients ≤25 years with POI attending a tertiary adolescent gynaecology service between 20202023. Patients with POI without identified cause and no other conditions/ treatments known to impact BMD were included. Data are reported as mean ± SD; group comparisons used Welch’s t tests and Fisher’s exact tests, and linear regression explored relationships between variables.

Results: 39 patients were identified: 27/39 (69%) with primary and 12/39 (31%) secondary amenorrhoea. Age at diagnosis was similar between groups (primary 16.0±2.3 vs secondary 15.5±2.2 years, P 0.53). Low BMD for age at the lumbar spine (Z ≤ 2.0) was observed in 59.0% (23/39), with a significant difference observed between primary (19/27, 70%) vs secondary (4/12, 33%) (P 0.012). In those with low BMD at the hip, there was no significant difference between groups (P 0.431). Lumbar spine Z-scores were not associated with age, height, vitamin D status, or duration of HRT exposure in either group. In primary amenorrhoea, lumbar spine BMD increased with weight (p 0.003), with no such association in secondary amenorrhoea (p 0.47). Age at menarche was significantly associated with lumbar spine Z scores in secondary amenorrhoea (p 0.003) but not age at first induced bleed in primary amenorrhoea (p 0.34).

Conclusion: POI presenting during adolescence is associated with significantly lower BMD. In this cohort, primary amenorrhoea was associated with significantly lower lumbar spine Z scores than secondary amenorrhoea, consistent with greater cumulative oestrogen deficiency prior to diagnosis and the critical role of sex steroids in peak bone mass accrual. These findings emphasise the need for timely diagnosis and treatment of POI. Future studies are needed to determine whether differences persist following completion of pubertal induction and define optimal pubertal induction and HRT regimens for adolescents with POI.