# Effectiveness of Daily Teriparatide in Managing Glucocorticoid-Induced Osteoporosis in Rheumatic Disease Patients After Switching From Bisphosphonate Therapy

**Authors:** Kaichi Kaneko, Makoto Kaburaki, Sei Muraoka, Kotaro Shikano, Nahoko Tanaka, Mai Kawazoe, Shinichi Kawai, Toshihiro Nanki

PMC · DOI: 10.7759/cureus.82471 · Cureus · 2025-04-17

## TL;DR

This study shows that switching from bisphosphonates to daily teriparatide improves bone density in patients with glucocorticoid-induced osteoporosis linked to rheumatic diseases.

## Contribution

The study provides new evidence that teriparatide is effective in increasing bone mineral density in patients unresponsive to bisphosphonates.

## Key findings

- Daily teriparatide significantly increased lumbar spine bone mineral density after six months.
- Serum sRANKL levels decreased significantly, while OPG levels remained stable.
- Bone formation and resorption markers increased during teriparatide therapy.

## Abstract

Background: Osteoporosis is a serious complication of systemic glucocorticoid therapy. Bisphosphonates are commonly used to treat glucocorticoid-induced osteoporosis (GIOP) but may be ineffective. Teriparatide, a recombinant form of parathyroid hormone, stimulates bone formation and may be a promising alternative for patients who show an inadequate response to bisphosphonates. Nonetheless, evidence supporting the effectiveness of daily teriparatide in GIOP patients with an inadequate bisphosphonate response remains limited. Serum soluble receptor activator of nuclear factor-kappa B ligand (sRANKL) and osteoprotegerin (OPG) are important biomarkers of bone metabolism and may aid in understanding and treating various diseases. However, changes in serum sRANKL and OPG levels following the administration of teriparatide to GIOP patients remain unclear. Therefore, the present study investigated the effects of daily teriparatide on bone mineral density (BMD) and the biochemical markers of bone metabolism in rheumatic disease patients with GIOP.

Methods: This study included 23 patients with GIOP in rheumatic diseases. Patients were switched from oral bisphosphonates to daily teriparatide. Patients receiving a median daily dose of 5.0 mg of prednisolone were eligible for the present study. BMD at the lumbar spine was assessed before and six months after teriparatide therapy. Serum sRANKL, OPG, bone formation markers (bone alkaline phosphatase, osteocalcin, and procollagen type 1 N-terminal peptide), and bone resorption markers (crosslinked N-telopeptide of type I collagen and tartrate-resistant acid phosphatase isoform 5b) were measured during teriparatide therapy.

Results: Six months of treatment with teriparatide significantly increased lumbar spine BMD (before treatment 0.67 [0.60-0.74] and six months after treatment (0.71 {0.67-0.81} {median and interquartile range} g/cm2, p = 0.0337). Serum sRANKL levels significantly decreased after teriparatide therapy (0.07 {0.00-0.19} to 0.00 {0.00-0.07} pmol/L, p = 0.0182), while OPG levels remained unchanged (6.71 {5.79-8.13} to 7.18 {5.96-8.92} pmol/L, p = 0.588). The sRANKL/OPG ratio significantly decreased from baseline (0.62 {0.00-3.08}) to after teriparatide therapy (0.00 {0.00-0.11}, p = 0.0287). All serum bone formation markers and bone resorption markers increased after teriparatide therapy. No new vertebral fractures were detected.

Conclusions: Switching from bisphosphonates to daily teriparatide significantly increased lumbar spine BMD in rheumatic disease patients with GIOP. Sequential therapy with daily teriparatide after bisphosphonates may be an effective treatment for GIOP.

## Linked entities

- **Proteins:** BTF3P11 (basic transcription factor 3 pseudogene 11)
- **Chemicals:** teriparatide (PubChem CID 16133850), prednisolone (PubChem CID 5755)
- **Diseases:** osteoporosis (MONDO:0005298), glucocorticoid-induced osteoporosis (MONDO:0000757), rheumatic disease (MONDO:0005554)

## Full-text entities

- **Genes:** TNFRSF11B (TNF receptor superfamily member 11b) [NCBI Gene 4982] {aka OCIF, OPG, PDB5, TR1}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, BGLAP (bone gamma-carboxyglutamate protein) [NCBI Gene 632] {aka BGP, OC, OCN}
- **Diseases:** vertebral fractures (MESH:C535781), Rheumatic Disease (MESH:D012216), GIOP (MESH:D010024)
- **Chemicals:** prednisolone (MESH:D011239), Bisphosphonate (MESH:D004164), Teriparatide (MESH:D019379)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

23 references — full list in the complete paper: https://tomesphere.com/paper/PMC12085251/full.md

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Source: https://tomesphere.com/paper/PMC12085251