Nishida Sachiyo, Shigesawa Ikumi, Nagai Satoshi, Itoh Naoki, Masumori Naoya
The Department of Urology, Sapporo Medical Center, NTT East Corporation･The Department of Urology, Sapporo Medical University.
The Department of Endocrinology, Sapporo Medical Center, NTT East Corporation.
Hinyokika Kiyo. 2021 Jan;67(1):47-51. doi: 10.14989/ActaUrolJap_67_1_47.
A 53-year-old man was diagnosed with prostate cancer with multiple bone metastasis. Therefore androgen deprivation therapy was initiated. After treatment with denosumab injection for bone metastasis, hypocalcemia and hypophosphatemia occurred. Despite treatment for hypocalcemia with vitamin D and calcium lactate,his serum calcium and phosphate levels were refractory to treatment. The etiology of hypophosphatemia was investigated,and the level of serum fibroblast growth factor 23 (FGF23) was abnormally elevated. Three months after the first measurement of FGF23,the patient died of prostate cancer. Severe hypophosphatemia is a typical manifestation of tumor-induced hypophosphatemic osteomalacia (TIO),which is a paraneoplastic condition, mediated by FGF23 overexpression in most cases. His osteoblastic metastasis,however,did not meet the disease criteria of osteomalacia. Several reports have suggested that excessive FGF23 may mediate both severe hypophosphatemia and aggressive castrationresistant prostate cancer characteristics. Management of serum FGF23 may be a novel therapeutic strategy for castration-resistant prostate cancer with hypophosphatemia.
一名53岁男性被诊断为前列腺癌伴多发骨转移。因此开始进行雄激素剥夺治疗。在使用地诺单抗注射治疗骨转移后，出现了低钙血症和低磷血症。尽管使用维生素D和乳酸钙治疗低钙血症，但其血清钙和磷水平对治疗无效。对低磷血症的病因进行了调查，发现血清成纤维细胞生长因子23（FGF23）水平异常升高。首次检测FGF23三个月后，患者死于前列腺癌。严重低磷血症是肿瘤诱导的低磷性骨软化症（TIO）的典型表现，TIO是一种副肿瘤性疾病，在大多数情况下由FGF23过度表达介导。然而，他的成骨性转移并不符合骨软化症的疾病标准。有几份报告表明，过量的FGF23可能介导严重低磷血症和侵袭性去势抵抗性前列腺癌的特征。管理血清FGF23可能是治疗伴有低磷血症的去势抵抗性前列腺癌的一种新的治疗策略。
