Tumor-induced osteomalacia
Tumor-induced osteomalacia
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DOI：
10.1002/art.23278
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发表时间：
2008-03-01
影响因子：
--
通讯作者：
Williams, Ralph C., Jr.
中科院分区：
文献类型：
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作者：
Lewiecki, E. Michael;Urig, Edward J., Jr.;Williams, Ralph C., Jr.
肿瘤诱导的骨软化症是一种罕见的获得性代谢紊乱，其特征是低磷血症和血清中1,25-二羟基维生素d水平过低。症状包括慢性肌肉和骨骼疼痛、虚弱和疲劳，与骨软化症引起脆性骨折的高风险相关。由于所呈现症状的非特异性，在血液化学测试中未能包括血清磷水平的测定，以及难以确定负责的肿瘤，诊断通常会延迟数年。肿瘤诱导的骨软化的发病机制涉及肿瘤中纤维母细胞生长因子23的表达，这种激素抑制近端肾小管对磷酸盐的重吸收，并下调肾脏中25-羟基维生素D向活性形式1,25-二羟基维生素D的转化。通过补充磷酸盐和骨化三醇可以部分或完全纠正代谢异常。明确的诊断和治疗需要切除肿瘤。
Tumor-induced osteomalacia is a rare acquired metabolic disorder characterized by hypophosphatemia and inappropriately low serum levels of 1,25-dihydroxyvitamin D. Symptoms include chronic muscle and bone pain, weakness, and fatigue in association with a high risk of fragility fractures due to osteomalacia. The diagnosis is commonly delayed for years due to the nonspecific nature of the presenting symptoms, failure to include determination of serum phosphorus levels in blood chemistry testing, and difficulty in identifying the responsible tumor. The pathogenesis of tumor-induced osteomalacia involves tumor expression of fibroblast growth factor 23, a hormone that inhibits proximal renal tubular reabsorption of phosphate and downregulates renal conversion of 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D. The metabolic abnormalities may be partially or,completely corrected with phosphate supplementation and calcitriol. A definitive diagnosis and treatment require excision of the responsible tumor.