Biochemical studies reveal hypophosphatemia (low blood phosphate), elevated alkaline phosphatase and low serum 1, 25 dihydroxyvitamin D levels. Routine laboratory tests may not include serum phosphate levels and this can result in considerable delay in diagnosis. Even when low phosphate is measured, its significance is often overlooked. The next most appropriate test is measurement of urine phosphate levels. If there is inappropriately high urine phosphate (phosphaturia) in the setting of low serum phosphate (hypophosphatemia), there should be a high suspicion for tumor-induced<unk> . FGF23 (see below) can be measured to confirm the diagnosis but this test is not widely available. Once hypophosphatemia and phosphaturia have been identified, begin a search for the causative tumor, which may be small and difficult to detect. Gallium-68 DOTA-Octreotate (DOTA-TATE) positron emission tomography (PET) scanning is the best way to locate these tumors. If this scan is not available, other options include Indium-111 Octreotide (Octreoscan) SPECT/CT, whole body CT or MRI imaging. Differential diagnosis Serum chemistries are identical in tumor-induced<unk> , X-linked hypophosphatemic rickets (XHR) and autosomal dominant hypophosphatemic rickets (ADHR). A negative family history can be useful in distinguishing tumor induced<unk>  from XHR and ADHR. If necessary, genetic testing for PHEX (phosphate regulating gene with homologies to endopeptidase on the X-chromosome) can be used to conclusively diagnose XHR and testing for the FGF23 gene will identify patients with ADHR.
Oncogenic osteomalacia
Metabolic bone disease
Endocrine bone disease
Vitamin D toxicity
Secondary hyperparathyroidism
Steroid-induced osteoporosis
Tertiary hyperparathyroidism
Normophosphatemic familial tumoral calcinosis