# Bone Mineral Density and Bone Quality Trends in a Child on Steroid Therapy Who Developed a Vertebral Fracture: A Case Report

**Authors:** Jun Aoyagi, Takahiro Kanai, Takane Ito, Marika Ishii, Toshihiro Tajima

PMC · DOI: 10.7759/cureus.82675 · 2025-04-21

## TL;DR

A child on steroid therapy developed a spine fracture, and monitoring bone markers helped guide treatment to prevent further fractures.

## Contribution

This case demonstrates how bone turnover markers can guide antiresorptive treatment duration in pediatric GIOP.

## Key findings

- Bone resorption markers increased while bone formation markers decreased before vertebral fractures occurred.
- Antiresorptive therapy normalized bone markers and increased bone mineral density.
- Serial monitoring of BMD and BTMs helped guide treatment cessation without further fractures.

## Abstract

Glucocorticoids (GCs) are commonly used to treat kidney problems in children and usually work well, but they can sometimes cause bone thinning, which may lead to fractures in the spine. Despite this, there is currently no established clinical approach for managing GC-induced osteoporosis (GIOP) in pediatric patients, highlighting the need for more data. Bone strength reflects both bone mineral density (BMD) and bone quality, with BMD assessed by X-ray and bone quality evaluated through serum or urine bone turnover markers (BTMs). In this case, a seven-year-old girl diagnosed with Henoch-Schönlein purpura nephritis was monitored over a two-year period during steroid treatment. Her BMD and serum BTMs, including alkaline phosphatase (ALP), tartrate-resistant acid phosphatase 5b (TRACP-5b), and undercarboxylated osteocalcin (ucOC), were tracked throughout the course. One month after initiating steroid therapy, her serum ALP (S-ALP) level decreased by 27.1% from baseline, while serum TRACP-5b (S-TRACP-5b) and serum ucOC increased by 34.4% and 52.3%, respectively, although BMD remained unchanged. Two months into treatment, she developed thoracic vertebral fractures (VFs) and was diagnosed with GIOP, prompting the initiation of oral alendronate sodium hydrate. Following the introduction of antiresorptive therapy and a reduction in GC dosage, both S-ALP and S-TRACP-5b levels returned to baseline by six months, accompanied by an 8.8% increase in BMD compared to the one-month level. No further fractures were observed after the cessation of antiresorptive treatment, which was guided by serial monitoring of BMD and BTMs. This case underscores the association of VFs with a decline in bone formation markers and elevations in bone resorption and matrix-related markers and demonstrates how BTMs reflecting bone quality can aid in determining the optimal duration of antiresorptive treatment in pediatric patients with GIOP.

## Linked entities

- **Chemicals:** alendronate sodium hydrate (PubChem CID 2088)
- **Diseases:** osteoporosis (MONDO:0005298)

## Full-text entities

- **Genes:** ALPP (alkaline phosphatase, placental) [NCBI Gene 250] {aka ALP, PALP, PLAP, PLAP-1}, ACP5 (acid phosphatase 5, tartrate resistant) [NCBI Gene 54] {aka HPAP, TRACP5a, TRACP5b, TRAP, TRAcP, TrATPase}
- **Diseases:** Henoch-Schönlein purpura nephritis (MESH:D011695), kidney problems (MESH:D007674), fractures in the spine (MESH:D000092443), fractures (MESH:D050723), VFs (MESH:C535781), GIOP (MESH:D010024)
- **Chemicals:** Steroid (MESH:D013256), alendronate sodium hydrate (MESH:D019386)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12093281/full.md

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Source: https://tomesphere.com/paper/PMC12093281