RA is associated with negative effects on both cortical and cancellous bone in postmenopausal women treated with bisphosphonates. Cortical geometric properties are also adversely affected mainly by increased endosteal circumference, whereas trabecular geometric properties are generally preserved.

Development of secondary or even tertiary hyperparathyroidism following phosphate administration is an established complication in patients with X-linked hypophosphatemic rickets. However, in tumor-induced osteomalacia (TIO) there are very few documented cases of hyperparathyroidism persisting even after excision of the tumor (tertiary hyperparathyroidism). The development of hyperparathyroidism in TIO is related to long-term phosphate administration, which represents the main treatment option in cases of unlocalized or nonexcisable tumors. Furthermore, low or inappropriately normal calcitriol levels either systemically or at the level of parathyroid cell are probably implicated in parathyroid tumorigenesis. We present a case of a 68year-old female patient with TIO who received long-term phosphate treatment prior to localization and excision of the tumor and afterward developed autonomous hyperparathyroidism. Learning Objectives• List the clinical and laboratory abnormalities characteristic of tumor-induced osteomalacia (TIO) as exemplified by the present patient.• Compare and contrast suggested mechanisms of hyperparathyroidism in patients with TIO. • Outline those therapeutic and follow-up strategies for patients with TIO that are most likely to prevent or minimize autonomous hyperparathyroidism.