Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Genetics Unit, Shriners Hospital for Children and McGill University, Montreal, QC, Canada.
J Bone Miner Res. 2019 Dec;34(12):2183-2191. doi: 10.1002/jbmr.3843. Epub 2019 Oct 1.
In adults with X-linked hypophosphatemia (XLH), excess FGF23 impairs renal phosphate reabsorption and suppresses production of 1,25-dihydroxyvitamin D, resulting in chronic hypophosphatemia and persistent osteomalacia. Osteomalacia is associated with poor bone quality causing atraumatic fractures, pseudofractures, delayed fracture healing, and bone pain. Burosumab is a fully human monoclonal antibody against FGF23. UX023-CL304 is an ongoing, open-label, single-arm, phase 3 study investigating the efficacy of subcutaneous burosumab, 1.0 mg/kg administered every 4 weeks, in improving osteomalacia in adults with XLH who have not been treated for at least 2 years before enrollment. The primary endpoint was improvement in osteoid volume/bone volume assessed by transiliac bone biopsies obtained at baseline and week 48. Additional assessments included serum phosphorus, markers of bone turnover, fracture/pseudofracture healing, and safety. Fourteen subjects enrolled, 13 completed 48 weeks, and 11 completed paired biopsies. All osteomalacia-related histomorphometric measures improved significantly at week 48 (mean percent change: osteoid volume/bone volume, -54%, osteoid thickness, -32%, osteoid surface/bone surface, -26%, [median] mineralization lag time, -83%). Mean serum phosphorus concentration averaged across the mid-point of the dose cycle between weeks 0 and 24 was 3.3 mg/dL, a 50% increase from 2.2 mg/dL at baseline. Markers of bone formation and resorption increased at week 48 (least squares [LS] mean increase: P1NP, +77%; CTx, +36%; both p < 0.0001). All subjects had one or more treatment-emergent adverse event (AE). Most AEs were mild to moderate in severity. Two subjects experienced serious AEs (migraine; paresthesia) that were unrelated to treatment and resolved. Eleven subjects had 18 biopsy procedure-related AEs: 14 for pain, two for itch, and one each for headache and bandage irritation. No deaths or incidents of hyperphosphatemia occurred. In conclusion, by normalizing phosphate homeostasis, burosumab significantly improved osteomalacia in adults with XLH, which likely explains the improved fracture healing and amelioration of skeletal complications. © 2019 The Authors. Journal of Bone and Mineral Research published by American Society for Bone and Mineral Research.
在 X 连锁低磷血症(XLH)的成年人中,过量的 FGF23 会损害肾脏对磷酸盐的重吸收并抑制 1,25-二羟维生素 D 的产生,导致慢性低磷血症和持续性骨软化症。骨软化症与骨质量差有关,导致非外伤性骨折、假性骨折、骨折愈合延迟和骨痛。Burosumab 是一种针对 FGF23 的全人源单克隆抗体。UX023-CL304 是一项正在进行的、开放性、单臂、3 期研究,旨在评估皮下注射 1.0mg/kg 布罗索umab 每 4 周一次,能否改善至少 2 年未接受治疗的 XLH 成年患者的骨软化症。主要终点是通过基线和 48 周时获得的髂骨活检评估的类骨质体积/骨体积的改善。其他评估包括血清磷、骨转换标志物、骨折/假性骨折愈合以及安全性。14 名受试者入组,13 名完成 48 周,11 名完成配对活检。所有与骨软化症相关的组织形态计量学指标在第 48 周时均显著改善(平均百分比变化:类骨质体积/骨体积,-54%;类骨质厚度,-32%;类骨质表面/骨表面,-26%;[中位数]矿化滞后时间,-83%)。在第 0 周到 24 周的剂量周期中点,平均血清磷浓度为 3.3mg/dL,比基线时的 2.2mg/dL 增加了 50%。骨形成和吸收标志物在第 48 周时增加(最小二乘[LS]均值增加:P1NP,+77%;CTX,+36%;均 p<0.0001)。所有受试者均发生了 1 次或多次治疗后出现的不良事件(AE)。大多数 AE 的严重程度为轻度至中度。2 名受试者发生了 2 次严重 AE(偏头痛;感觉异常),与治疗无关,且已痊愈。11 名受试者出现了 18 次与活检程序相关的 AE:14 次为疼痛,2 次为瘙痒,1 次为头痛,1 次为绷带刺激。无死亡或高磷血症发生。总之,通过使磷酸盐稳态正常化,布罗索umab 显著改善了 XLH 成年患者的骨软化症,这可能解释了骨折愈合的改善和骨骼并发症的缓解。 © 2019 美国骨矿研究协会。