Department of Metabolism, Endocrinology, and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan.
Division of Nephrology and Endocrinology, The University of Tokyo Hospital, Tokyo, Japan.
J Bone Miner Res. 2021 Feb;36(2):262-270. doi: 10.1002/jbmr.4184. Epub 2020 Nov 4.
Patients with tumor-induced osteomalacia (TIO), an acquired paraneoplastic condition characterized by osteomalacia due to hypophosphatemia, exhibit a similar clinical picture to those with X-linked hypophosphatemic rickets/osteomalacia (XLH). The human monoclonal anti-fibroblast growth factor 23 (FGF23) antibody burosumab (KRN23) increases serum phosphate and improves bone turnover, fracture healing, pain, and physical function in XLH patients by inhibiting circulating FGF23; thus, burosumab is expected to be an effective treatment for TIO. We report here an interim analysis of a multicenter, open-label, intraindividual dose-adjustment study of burosumab (0.3 to 2.0 mg/kg every 4 weeks) in Japanese and Korean TIO patients. The primary endpoint was the fasting serum phosphate level at each visit. Key secondary endpoints were changes over time in bone biomarkers, pharmacodynamic markers, bone histomorphometric parameters, motor function, and patient-reported outcomes. Safety was assessed based on treatment-emergent adverse events (TEAEs). Thirteen patients received burosumab treatment, of whom 4 underwent bone biopsy. The mean dose after week 112 was approximately 1.0 mg/kg. After the first burosumab administration, mean serum phosphate levels increased and remained above the lower limit of normal and in the normal range from weeks 14 to 112. Bone biomarkers initially increased, reaching maximum values at week 16 or 24, and then gradually decreased. After burosumab treatment, patients were able to walk further (evaluated by the 6-minute walk test), reported decreased pain levels, and showed a tendency toward healing of baseline fractures and pseudofractures. Two patients discontinued, one each due to disease progression and consent withdrawal. Burosumab was generally well tolerated, with no treatment-related TEAEs of grade ≥3 and no treatment-related serious AEs. In conclusion, the interim results of this first study of burosumab to treat TIO patients indicate that this drug has the potential to provide clinical benefit for patients with unresectable tumors. The full study results are eagerly anticipated. © 2020 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR)..
肿瘤相关性骨软化症(TIO)患者存在低磷血症导致的佝偻病/骨软化症(XLH),其临床表现与 XLH 患者相似。人源化抗成纤维细胞生长因子 23(FGF23)单克隆抗体布罗索尤单抗(KRN23)通过抑制循环 FGF23 增加血清磷酸盐并改善骨转换、骨折愈合、疼痛和 XLH 患者的身体功能;因此,布罗索尤单抗有望成为 TIO 的有效治疗方法。我们在此报告了一项多中心、开放标签、个体内剂量调整研究的中期分析,该研究评估了布罗索尤单抗(每 4 周 0.3 至 2.0mg/kg)在日本和韩国 TIO 患者中的疗效。主要终点是每次就诊时的空腹血清磷酸盐水平。次要终点是骨生物标志物、药效学标志物、骨组织形态计量学参数、运动功能和患者报告结局的随时间变化。根据治疗出现的不良事件(TEAEs)评估安全性。13 名患者接受了布罗索尤单抗治疗,其中 4 名患者进行了骨活检。第 112 周后的平均剂量约为 1.0mg/kg。首次布罗索尤单抗给药后,平均血清磷酸盐水平升高并持续高于下限正常范围,并在第 14 至 112 周保持在正常范围内。骨生物标志物最初升高,在第 16 或 24 周达到最大值,然后逐渐下降。布罗索尤单抗治疗后,患者能够走得更远(通过 6 分钟步行测试评估),报告疼痛水平降低,并且基线骨折和假骨折有愈合趋势。2 名患者因疾病进展和同意退出而停药。布罗索尤单抗总体耐受性良好,无治疗相关的≥3 级 TEAEs,也无治疗相关的严重不良事件。总之,这项布罗索尤单抗治疗 TIO 患者的首次研究的中期结果表明,该药物有可能为无法切除肿瘤的患者带来临床获益。我们热切期待完整的研究结果。