Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome usually caused by small-sized tumors. Tumors secrete fibroblast growth factor 23 (FGF23), which has a phosphaturic effect. The clinical signs of TIO are non-specific, and include fatigue, bone pain and muscle weakness, which makes timely diagnosis of the disease difficult and treatment is often delayed. Well-timed diagnosis is essential and combined with complete tumor resection it leads to complete relief of symptoms and good postoperative prognosis. In cases of undetected tumors, medical treatment with phosphate supplements and active vitamin D medications is usually successful, however, treatment is associated with numerous complications and side effects can be burdensome for the patients. Due to the risk of recurrence or metastasis, patients with TIO require long-term management and follow-up. In this article, we present a clinical case of successful diagnosis and treatment of TIO in a young patient with type 1 diabetes mellitus.

Hypoparathyroidism is a rare disorder characterized by parathyroid hormone (PTH) insufficiency, the development of hypocalcemia and alteration of bone tissue remodeling. The goal of treatment is to normalize the indicators of calcium-phosphorus metabolism and leveling of clinical manifestations. Standard treatment of hypoparathyroidism consists of oral calcium and active forms of vitamin D, in doses necessary to maintain calcium levels at the lower limit of the reference interval. Nevertheless, treatment of the disease exerts certain difficulties in clinical practice. At the same time, compensation of the hypoparathyroidism is necessary to prevent ectopic calcification. Daily subcutaneous delivery of PTH (1–84) and PTH (1–34) has emerged as a promising therapeutic tool. However, its use should be restricted to patients insufficiently controlled with the standard treatment with active vitamin D and calcium. We present a clinical case of idiopathic hypoparathyroidism with severe clinical presentation of hypocalcaemia and ectopic calcification. Idiopathic hypoparathyroidism is a consequence of autoimmune destruction of the parathyroid glands and is exhibited by excluding all known causes of hypoparathyroidism. PTH (1–34) treatment allowed reducing the dose of calcium and vitamin D and achieving compensation of the disease.