腎と骨代謝 Vol.27 No.1(9)


特集名 腫瘍と骨ミネラル代謝
題名 腫瘍性骨軟化症とFGF23
発刊年月 2014年 01月
著者 福本 誠二 東京大学医学部附属病院腎臓・内分泌内科
【 要旨 】 腫瘍性骨軟化症（tumor-induced osteomalacia；TIO）は，腫瘍随伴症候群の一つである．TIOの惹起因子としても同定された線維芽細胞増殖因子23（fibroblast growth factor 23；FGF23）は，腎近位尿細管リン再吸収と，1,25-水酸化ビタミンD濃度の低下を介する腸管リン吸収の抑制から，低リン血症を惹起する．TIO惹起腫瘍はFGF23を過剰産生し，TIO患者の血中FGF23濃度は高値を示す．また原因腫瘍の完全摘除により，血中FGF23は速やかに低下し，TIOは完治する．一方腫瘍の発見できない例など，TIO惹起腫瘍が摘除できない症例に対しては，FGF23活性を阻害する方法が新たな治療法として考えられている．
Theme Tumors and bone mineral metabolism
Title Tumor-induced osteomalacia and FGF23
Author Seiji Fukumoto Division of Nephrology & Endocrinology, Department of Medicine, University of Tokyo Hospital
[ Summary ] Tumor-induced osteomalacia is one of paraneoplastic syndromes. Fibroblast growth factor 23 (FGF23) which was identified as a causative factor for TIO reduces serum phosphate by inhibiting proximal tubular phosphate reabsorption and intestinal phosphate absorption by reducing 1,25-dihydroxyvitamin D level. It has been reported that tumors responsible for TIO overexpress FGF23. In addition, patients with TIO exhibit high circulatory levels of FGF23 and this elevated FGF23 rapidly decreases after resection of responsible tumors for TIO. TIO is cured by complete removal of responsible tumors. On the other hand, several methods to inhibit FGF23 activity are considered as novel therapeutic measures for patients with TIO whose tumors cannot be removed.
戻る