MON-785 Vertebral Osteosclerosis In Secondary Hyperparathyroidism

Abstract Disclosure: Y. Ding: None. B. Phillips: None. Introduction: Secondary hyperparathyroidism (SHPT) is characterized by an increased secretion of parathyroid hormone (PTH) in response to stimuli such as hypocalcemia, hyperphosphatemia, or decreased levels of active vitamin D. The most frequent causes of SHPT are vitamin D deficiency and chronic kidney disease. PTH is a major regulator of osteoclast activity and bone remodeling. Typical bone manifestations of hyperparathyroidism include diffuse osteopenia, brown tumors, subperiosteal bone resorption, pathological fractures, terminal acro-osteolysis, and salt-and-pepper skull. Osteosclerotic changes are an uncommon feature of hyperparathyroidism and have been rarely reported. We describe a case of vertebral osteosclerosis in a patient with SHPT. Case Presentation A 59-year-old Caucasian man presented with generalized bone pain and tenderness, prominently in his back. Laboratory tests revealed hypocalcemia (serum calcium of 6.8 mg/dL), hypophosphatemia (serum phosphorus of 1.2 mg/dL), elevated alkaline phosphatase (230 IU/L), and extremely low 25-OH Vitamin D level (<4 ng/mL). Serum intact PTH increased significantly to 990 pg/mL. Further investigation of his prior computed tomography (CT) of the thoracic and lumbar spines (6 months prior) discovered diffuse osteosclerosis of vertebral bodies without focal osteolytic or osteoblastic lesions. His renal function tests at that time were within normal limits. Discussion: An elevated PTH with hypocalcemia is diagnostic of SHPT. In our case, SHPT is presumably caused by a combination of vitamin D deficiency and hypocalcemia, as vitamin D deficiency alone usually does not result in severe hyperparathyroidism. His normal baseline kidney function and hypophosphatemia negate the possibility of SHPT attributed to chronic kidney disease. Excess PTH stimulates osteoclast activity leading to increased bone resorption with subsequent fibrous replacement and reactive osteoblast activity. This process leads to characteristic radiological findings of osteopenia and osteolytic lesions. However, osteosclerosis is unusual in hyperparathyroidism. Although osteosclerosis has been reported in patients with primary hyperparathyroidism and renal SHPT, it is rare in those with nutritional SHPT. Furthermore, osteosclerotic changes in SHPT affect the skull more frequently than the spine. We present the case highlighting diffuse vertebral osteosclerosis in SHPT caused by vitamin D deficiency and hypocalcemia. The mechanism of hyperostosis in SHPT involves a complex interplay of increased PTH secretion and synthesis, an exaggerated osteoblastic response following prolonged osteoclastic activity, and activation of specific cellular pathways that promote parathyroid cell proliferation and bone turnover. Presentation: Monday, July 14, 2025