MON-742 Less is More: Successful Conservative Management of PTH-Independent Hypercalcemia Due to Vitamin D Toxicity

Abstract Disclosure: M.S. Martinez-Cruz: None. A. Qamar: None. Background: Vitamin D toxicity is a rare but recognized cause of PTH-dependent hypercalcemia. Despite the increasing use of vitamin D supplements in the past decade, cases remain infrequent, and management strategies for such cases are understudied. Case Description: A 25-year-old male presented to the emergency with intermittent nausea, vomiting, generalized weakness, polyuria, polydipsia, and anorexia. His medical history was significant for suspected autism spectrum disorder and unspecified psychosis, characterized by obsessive health-related concerns. He frequently watched online videos about bone health and self-administered high doses of vitamin D. His regimen included vitamin D3 25,000 IU twice daily, occasional additional doses of vitamin D3 50,000 IU daily, and one calcium-containing tablet three times daily (each containing 1,000 IU vitamin D, 1,000 mg calcium carbonate, and gluconate) for at least six months before presentation. On admission, he presented with severe PTH-independent hypercalcemia, with a corrected calcium (cCa) level of 16.3 mg/dL (reference: 8.7-10.2 mg/dL), ionized calcium of 1.99 mmol/L (reference: 1.15-1.32 mmol/L), and PTH 5 pg/mL (reference: 14-72 pg/mL). Initial management included aggressive intravenous fluids and discontinuation of calcium and vitamin D supplements. Laboratory testing revealed a markedly elevated 25-hydroxyvitamin D (25-OH D) level of 340 ng/mL by liquid chromatography, consistent with vitamin D toxicity. However, 1,25-dihydroxyvitamin D levels could not be determined due to an unknown interfering substance in the liquid chromatography assay. Once cCa improved to 12 mg/dL, we opted to discontinue intravenous fluids and encourage oral hydration. No additional pharmacologic interventions were initiated. Within six days, the patient’s calcium levels normalized, and one month after discharge, his serum corrected calcium remained stable at 9.9 mg/dL. Conclusion: The success of this conservative approach underscores the reliability of the finely regulated vitamin D metabolism, which prevents hypercalcemia through negative feedback mechanisms, including PTH suppression, stimulation of fibroblast growth factor 23 (FGF23) and α-Klotho, and subsequent suppression of CYP27B1 and induction of CYP24A1. Consequently, hypercalcemia in such cases may primarily be explained by excessive calcium intake or, less frequently, by polymorphisms/ mutations in CYP24A1. Presentation: Monday, July 14, 2025