肿瘤诱发骨软化症（TIO）是一种超级罕见的副肿瘤综合征，由于成纤维细胞生长因子23（FGF23）的过度产生而引起，在影响患者的发病率方面具有深远的影响。 TIO是一种常被漏诊的疾病，需要医生增强对其认识，以便及时和正确地管理患者。患有TIO的患者通常报告的症状是非特异性的，因此诊断难以确定，最初的误诊率超过95％。 TIO的生化特征由低磷血症、FGF23的升高或不当的正常水平以及1,25（OH）2D的降低或正常低循环水平表示。在大多数受影响的患者中，磷酸盐分化间充质肿瘤是TIO潜在的病理实体。现在有证据表明，FN1-FGFR1和FN1-FGF1融合基因存在于导致这种副肿瘤综合征的肿瘤约一半中。导致TIO的肿瘤通常很小且生长缓慢。它们可以在从头到脚的身体各个部位发生，软组织和骨骼中的患病率相似。有许多功能和解剖学成像技术可用于肿瘤定位；68Ga DOTA为基础的技术具有更好的敏感性。手术是首选的治疗方法；如果无法定位肿瘤或切除不完整，现在有多种医学治疗方法可供选择。©作者（S）2022。由牛津大学出版社代表内分泌学会出版。保留所有权利。有关权限，请发送电子邮件至：journals.permissions@oup.com。

Tumor-induced osteomalacia (TIO) is an ultrarare paraneoplastic syndrome due to overproduction of fibroblast growth factor 23 (FGF23), with profound effects on the morbidity of the patients affected. TIO is an underdiagnosed disease, whose awareness should be increased among physicians, for timely and proper management of the patients. Symptoms reported by patients with TIO are usually nonspecific thus rendering the diagnosis elusive, with an initial misdiagnosis rate of >95%. Biochemical features of TIO are represented by hypophosphatemia, increased or inappropriately normal levels of FGF23 and low to low normal circulating 1,25(OH)2D. Phosphaturic mesenchymal tumors are the pathological entities underlying TIO in most affected patients. There is now evidence that FN1-FGFR1 and FN1-FGF1 fusion genes are present in about half of tumors causing this paraneoplastic syndrome. Tumors causing TIO are often of small size and grow slowly. They can occur in all parts of the body from head to toe with similar prevalence in soft tissue and bone. There are a number of functional and anatomical imaging techniques utilized for tumor localization; 68Ga DOTA based technologies have the better sensitivity. Surgery is the treatment of choice; several medical treatments are now available in case of inability to locate the tumor or in case of incomplete excision.© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.