阿德福韦酯诱导的低磷骨软化症和骨质疏松症：病例报告和文献综述

摘要(中文译文)

阿德福韦酯（ADV）的肾毒性可诱发范可尼综合征，进而导致低磷性骨软化症。我们报告一例67岁绝经后女性患者，因慢性乙型肝炎长期接受阿德福韦酯治疗。她表现为严重骨痛和多发性假骨折，被诊断为药物诱导的低磷性骨软化症。停用阿德福韦并补充维生素D和磷酸盐后，其生化指标恢复正常，骨痛显著改善，表明骨软化症已基本纠正。然而，尽管随访骨密度（BMD）较治疗前值有显著改善，但仍明显低于同龄女性的参考范围。因此怀疑存在绝经后骨质疏松症，并在骨软化症纠正后启动了抗骨质疏松药物治疗。本病例提示，在药物诱导的骨软化症中，去除致病因素后骨密度可大幅改善；然而，若患者存在骨质疏松症的潜在危险因素，即使骨软化症缓解后低骨密度仍可能持续存在，需要进一步评估和干预。

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.

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