Tumor induced osteomalacia is a rare acquired disease. The cause is a mesenchymal tumor secreting fibroblast growth factor 23 (FGF23). An excessive amount of FGF 23 disrupts the metabolism of phosphorus and vitamin D, which leads to severe paraneoplastic syndrome, manifested in the form of multiple fractures, severe pain in the bones and generalized myopathy. With oncogenic osteomalacia, a complete cure is possible with radical resection of the tumor. Unfortunately, localization, small size of formations and rare frequency of occurrence lead to the fact that the disease remains unrecognized for a long time and leads to severe, disabling consequences. A step-by-step approach to diagnosis improves treatment outcomes. First, a thorough anamnesis is collected, then functional visualization is performed and the diagnosis is confirmed by anatomical visualization of the tumor. After that, the method of choice is a surgical treatment. If resection is not possible, then conservative therapy with active metabolites of vitamin D and phosphorus salts is indicated. New therapeutic approaches, such as the antibody to FGF23 or the pan-inhibitor of receptors to FGF, are actively developing. This article provides an overview of modern approaches to the diagnosis and treatment of this disease.

Primary hyperparathyroidism (PHPT) is characterized by hypercalcemia. The only curative treatment is parathyroidectomy. However, patients are often ineligible or decline surgery. Denosumab (Dmab) is an antiresorptive pharmaceutical alternative. The effects of exposure to Dmab in subjects with chronic kidney disease (CKD) and PHPT are unknown. Purpose:We aimed to assess the efficacy and safety of denosumab in postmenopausal women with PHPT- related osteoporosis and CKD. Methods: Women over 50 years of age with PHPT or postmenopausal osteoporosis (PMO) were retrospectively recruited into this longitudinal study. These PHPT and PMO groups were further categorized into four subgroups based on the presence of CKD (Glomerular filtration rate (GFR) <60 mL/min/1.73mBI): patients with PHPT with and without CKD and patients with PMO with and without CKD. All patients were given denosumab over 24 months due to verified osteoporosis. The primary outcomes were changes in bone mineral density (BMD) and serum calcium levels. Results: 145 postmenopausal women median age 69 [63;77] were recruited and assigned to one of the subgroups. Denosumab treatment significantly increased BMD (median ΔT-score: L1-L4 +0.65 (p<0.001), femur neck +0.3 (p=0.012); radius 33% +0.2 (p<0.05)) in PHPT-related osteoporosis and CKD at 24 months. Changes in BMD were similar in all study groups compared to baseline. A marked decline in calcium was noted in the primary study group of PHPT with CKD (median ΔCa = -0.24 mmol/L p<0.001), compared to PHPT without CKD (median ΔCa = -0.08 mmol/L p<0.001) and PMO with or without CKD. Denosumab treatment was well-tolerated with no serious adverse events. Conclusion: Denosumab treatment was similarly effective at increasing BMD in patients with PHPT and PMO with and without renal insufficiency. The calcium lowering effects of denosumab were most significant in patients with PHPT and CKD. The safety of denosumab did not differ among participants with and without CKD.