Prednisolone impairs trabecular bone score changes in adolescents with 21-hydroxylase deficiency.

Abstract

Background: Individuals with 21-hydroxylase deficiency (21OHD) require lifelong glucocorticoid (GC) therapy, which increases their risk of fragility fractures. However, fractures in GC-treated individuals can occur at normal bone mineral density (BMD) levels, suggesting an alteration in the bone microarchitecture.

Purpose: To evaluate trabecular bone microarchitecture and its changes in adolescents with 21OHD.

Methods: We enrolled 38 adolescents with 21OHD for whom complete clinical data and baseline and follow-up lumbar spine bone mineral density (LSBMD) measurements were available. The mean duration was 1.5 ± 0.6 years. Trabecular bone score (TBS), an indirect measurement of bone microarchitecture, was analyzed using iNsight™ software version 3.0. Impaired BMD and TBS were defined at Z-scores ≤ -1.5.

Results: At baseline, participants (55% female; 68% salt-wasting type; mean age, 15.2 ± 3.8 years; bone age, 17.5 ± 2.8 years; mean GC dose, 18.5 ± 6.5 mg/m2/day) had the prevalence of impaired BMD and TBS of 5% and 18%, respectively. During follow-up, adolescents with 21OHD receiving prednisolone showed a lower annual percentage change in TBS than those who received hydrocortisone (p = 0.028). A stepwise regression analysis showed that body mass index percentile (p < 0.001) and testosterone concentration (p = 0.002) were independent positive predictors of the baseline TBS Z-score, whereas prednisolone use was the only negative predictor of the annual percentage change in TBS (p = 0.002).

Conclusion: Adolescents with 21OHD have a high prevalence of impaired bone microarchitecture. Furthermore, prednisolone therapy is associated with impaired bone microarchitecture development, suggesting that hydrocortisone may better preserve bone microarchitecture and should be considered the first-line treatment for this population.