Wilkins G E, Granleese S, Hegele R G, Holden J, Anderson D W, Bondy G P
Department of Medicine, St. Paul's Hospital, Vancouver, British Columbia, Canada.
J Clin Endocrinol Metab. 1995 May;80(5):1628-34. doi: 10.1210/jcem.80.5.7745010.
Oncogenic osteomalacia is a syndrome characterized by phosphaturia, hypophosphatemia, reduced vitamin D levels, and osteomalacia. The cause is not known, but all patients have had a tumor; usually of mesenchymal origin. Removal of the tumor reverses the metabolic abnormalities. We report a patient with osteomalacia, severe hypophosphatemia, elevated alkaline phosphatase, low 1,25-dihydroxyvitamin D3, and phosphaturia. A tumor was identified in the infratemporal fossa. The tumor was removed, and all of the biochemical abnormalities resolved over the subsequent 8 months. The bone density returned to normal values. The tumor had the appearance of a paraganglioma and was used to establish a cell culture line called JH-55. Electron microscopy of the original tumor and the JH-55 cells demonstrated the presence of neurosecretory granules. A bioassay using opossum kidney cells was used to evaluate phosphate transport. Conditioned medium from the JH-55 cells inhibited phosphate reabsorption by the kidney tubular cells. Maximal inhibition required a 24-h incubation period and was not altered by the presence of an inhibitor of protein synthesis (10 micrograms/mL cycloheximide). Immunoassays revealed no detectable PTH-related peptide or intact PTH in the JH-55 medium. The cause of this paraneoplastic syndrome is not known, but all of the evidence is consistent with the action of a hormone that produces phosphaturia. This putative factor is distinct from other hormones that cause phosphaturia.
致癌性骨软化症是一种以磷尿症、低磷血症、维生素D水平降低和骨软化症为特征的综合征。病因不明,但所有患者都有肿瘤,通常起源于间充质。切除肿瘤可逆转代谢异常。我们报告了一名患有骨软化症、严重低磷血症、碱性磷酸酶升高、1,25-二羟维生素D3降低和磷尿症的患者。在颞下窝发现了一个肿瘤。切除肿瘤后,所有生化异常在随后8个月内得到解决。骨密度恢复到正常水平。该肿瘤外观为副神经节瘤,并被用于建立一个名为JH-55的细胞系。对原始肿瘤和JH-55细胞进行电子显微镜检查显示存在神经分泌颗粒。使用负鼠肾细胞进行生物测定以评估磷酸盐转运。JH-55细胞的条件培养基抑制肾小管细胞对磷酸盐的重吸收。最大抑制作用需要24小时的孵育期,并且不受蛋白质合成抑制剂(10微克/毫升环己酰亚胺)的影响。免疫测定显示JH-55培养基中未检测到甲状旁腺激素相关肽或完整的甲状旁腺激素。这种副肿瘤综合征的病因尚不清楚,但所有证据都与一种导致磷尿症的激素的作用一致。这种假定的因子与其他导致磷尿症 的激素不同。