Tumor-Induced Osteomalacia

Beur, Suzanne M. Jan de

doi:10.1001/jama.294.10.1260

Cited by 219 publications

(207 citation statements)

References 111 publications

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“…Treatment should be maintained until surgical removal of the tumor. Biochemical abnormalities and symptoms of the patient resolve rapidly with removal (Jan de Beur , 2005).…”

Section: Expectations Of Response From Octreotide Therapy In Recurrentmentioning

confidence: 99%

Expectations of Response from Octreotide Therapy in Recurrent Phosphaturic Mesenchymal Tumors - Do They Reflect Reality?

Ulaş

Dede²,

Şendur³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…Treatment should be maintained until surgical removal of the tumor. Biochemical abnormalities and symptoms of the patient resolve rapidly with removal (Jan de Beur , 2005).…”

Section: Expectations Of Response From Octreotide Therapy In Recurrentmentioning

confidence: 99%

Expectations of Response from Octreotide Therapy in Recurrent Phosphaturic Mesenchymal Tumors - Do They Reflect Reality?

Ulaş

Dede²,

Şendur³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…An increased secretion of fibroblast growth factor-23 (FGF-23) is considered the pathological factor responsible for the disease (2,3). The awareness of the disease has recently increased (4), even though no more than 300 cases have been described so far (5,6).…”

Section: Introductionmentioning

confidence: 99%

Six-year follow-up of a characteristic osteolytic lesion in a patient with tumor-induced osteomalacia

Piemonte

Romagnoli

Cipriani

et al. 2014

European Journal of Endocrinology

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Objective: Tumor-induced osteomalacia is a rare paraneoplastic syndrome characterized by hypophosphatemia and inappropriately normal or low 1,25-dihydroxyvitamin D. Clinical case: Here, we report a 6-year postoperative follow-up of a patient with oncogenic osteomalacia with a distinctive skeletal manifestation. The latter was characterized by an almost linear lytic lesion of a few millimeters with irregular borders, mainly involving the trabecular compartment but extending into cortical shell, located in the middle third of the right fibula. Six years after tumor resection, a sclerotic repair with a complete recovery was observed. Furthermore, we monitored a striking increase in bone mineral density throughout the observation period, reaching a peak of 73% over basal values at lumbar spine after 2 years; at total femur and radius, the peak was 47.5 and 4.6% respectively, after 4 years from tumor resection. Conclusions: We report for the first time that an osteolytic lesion may be part of the skeletal involvement in tumor-induced osteomalacia.

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“…It is generally recognized that PTH and vitamin D are the key regulators of phosphate metabolism. However, several novel regulators of phosphate homeostasis have been identified as being associated with hypophosphatemia of various types, such as tumor-induced osteomalacia, several hereditary forms of hypophosphatemic rickets, X-linked hypophosphatemia, and autosomal dominant hypophosphatemia (1,3 ). Oncogenic hypophosphatemia is a rare cause of severe hypophosphatemia.…”

Section: Discussionmentioning

confidence: 99%

Severe Hypophosphatemia in a 79-Year-Old Man

Meng

Wagar

2014

Clinical Chemistry

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A 79-year-old white man with a history of progressive bone pain was admitted for evaluation 3 years ago. The patient reported that the pain began in both feet and gradually spread to the rest of the body over a 2-year period. Further assessment revealed multiple stress fractures in the feet. Bone mineral density test indicated osteopenia. Serial bone mineral density tests during the 2 years showed that his osteopenia was progressing. Results of several serum protein electrophoreses were essentially normal. His medical history, which included surgical removal of a cerebral aneurysm near the sella turcica and bacterial meningitis, suggested no pertinent etiologic factors. Physical examination revealed no clinically significant findings except unsteady gait. His serum phosphate concentrations declined from 2.5 to 1.8 mg/dL over the 2 years before admission. Laboratory test results at the time of admission are summarized in Table 1. The patient's phosphate concentration reached a nadir of 1.2 mg/dL at admission. His serum alkaline phosphatase was increased. Other notable abnormalities included low normal calcium, normal to borderline high parathyroid hormone (PTH), 2 and increased 24-h urine phosphate and calcium excretion. Other routine biochemical parameters [including ionized calcium, thyroid-stimulating hormone, and free thyroxine (T 4 )] were normal. The patient underwent a whole-body scan showing multiple bone lesions. Diagnostic imaging studies including x-ray, a computer axial tomography (CAT), and MRI of the lungs, abdomen, and pelvis were reported to be normal at admission.Based on the above findings, the patient was diagnosed with osteomalacia secondary to hypophosphatemia. He was then treated with several medications, including bisphosphonates, calcitriol, vitamin D, and calcium and phosphorus supplements. Vitamin D was given because his initial calcium and phosphate concentrations were low, and it was discontinued later following improvement of serum calcium concentrations. Despite substantial phosphorus replacement (250 mg phosphorus per tablet, 2 tablets 3 times a day), the hypophosphatemia continued, along with bone fragility and muscle weakness over the next 3 years, and his height decreased from 173 to 163 cm. DISCUSSIONThe patient was evaluated further by several physicians from different disciplines 3 years after the first admission. This evaluation revealed extensive bone lesions and multiple rib fractures consistent with osteomalacia. In addition, he was found to have a soft tissue mass on the left posterior 10th rib, and computed tomography (CT) scan revealed cortical destruction of this rib. Follow-up MRI showed a mass suggesting expansile hemangiopericytoma of the left posterior thorax. CTguided fine-needle aspiration biopsy and histologic evaluation of the sample confirmed hemangiopericytoma. His plasma concentration of fibroblast growth factor 23 (FGF23) was increased (292 RU/mL; reference interval Յ180 RU/mL). A diagnosis of hemangiopericytoma with secondary tumor-induced osteomalacia and...

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Tumor-Induced Osteomalacia

Cited by 219 publications

References 111 publications

Expectations of Response from Octreotide Therapy in Recurrent Phosphaturic Mesenchymal Tumors - Do They Reflect Reality?

Expectations of Response from Octreotide Therapy in Recurrent Phosphaturic Mesenchymal Tumors - Do They Reflect Reality?

Six-year follow-up of a characteristic osteolytic lesion in a patient with tumor-induced osteomalacia

Severe Hypophosphatemia in a 79-Year-Old Man

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