# Adefovir dipivoxil-induced hypophosphatemic osteomalacia and osteoporosis: a case report and literature review

## TL;DR

A 67-year-old woman on adefovir dipivoxil developed bone issues, which improved after stopping the drug, but low bone density persisted due to underlying osteoporosis.

## Contribution

This case highlights the importance of monitoring and managing osteoporosis risk after resolving drug-induced osteomalacia.

## Key findings

- Discontinuation of adefovir and supplementation improved biochemical parameters and bone pain.
- Bone mineral density improved but remained below normal, suggesting underlying osteoporosis.
- Anti-osteoporotic treatment was initiated after resolving osteomalacia.

## Abstract

The nephrotoxicity of adefovir dipivoxil (ADV) can induce Fanconi syndrome, which causes hypophosphatemic osteomalacia. We report a case of a 67-year-old postmenopausal woman who had been receiving long-term adefovir dipivoxil therapy for chronic hepatitis B. She presented with severe bone pain and multiple pseudofractures, and was diagnosed with drug-induced hypophosphatemic osteomalacia. Following discontinuation of adefovir and supplementation with vitamin D and phosphate, her biochemical parameters normalized and bone pain significantly improved, indicating that osteomalacia had been essentially corrected. However, although follow-up bone mineral density (BMD) showed significant improvement compared to pretreatment values, it remained markedly below the reference range for age-matched women. Postmenopausal osteoporosis was therefore suspected, and anti-osteoporotic pharmacotherapy was initiated after correction of osteomalacia. This case suggests that BMD can improve substantially after removal of the causative factor in drug-induced osteomalacia; however, if patients have underlying risk factors for osteoporosis, low BMD may persist even after osteomalacia resolution, necessitating further evaluation and intervention.