SAT-714 Bone Appétit: A Case Of Hungry Bone Syndrome In Prostate Cancer

Abstract Disclosure: C. Quintana-Ocasio: None. M. Santos-Lopez: None. N. Vergne-Santiago: None. G. Feliciano-Diaz: None. Hungry bone syndrome is a well recognized metabolic disease characterized by excessive calcium and phosphorus sequestration in the bone, manifesting as hypocalcemia and hypophosphatemia. It is most commonly seen as a complication of parathyroidectomy in patients with long standing primary hyperparathyroidism. Prostate cancer is the most common cancer among males in the US and its the second-leading cause of cancer-related death. Hungry bone syndrome can be a rare complication of metastatic prostate malignancy but its exact incidence is not clearly established in the medical literature. An 80-year-old male with a complex medical history consisting of metastatic prostate cancer on active chemotherapy and chronic kidney disease (CKD) who was admitted to the hospital with complicated urinary tract infection. He exhibited symptoms of fatigue, perioral numbness, and muscle cramps. Case was complicated after developing a generalized tonic-clonic seizure requiring endotracheal intubation. Further work up revealed persistent hypocalcemia. Electrocardiogram presented a prolonged QT interval. Laboratory evaluation demonstrated severe hypocalcemia (corrected non-ionized calcium 3.4 mg/dL) and low ionized calcium (3 mg/dL [4.5 - 5.6 mg/dL]), elevated alkaline phosphatase 353 u/L [46 - 116 u/L], with elevated parathyroid hormone levels 446 pg/dL [18.5 - 88 pg/dL]. Extensive osteoblastic bone metastases were confirmed on imaging. During hospitalization, hypocalcemia was refractory necessitating multiple intravenous calcium infusion, calcitriol and cholecalciferol. He was discharged on calcium carbonate 600 mg 2 tablets TID, calcitriol 2 mcg BID and an extra 1000 mg of elemental calcium at bedtime. Hypocalcemia in the context of metastatic prostate cancer can be explained by increased sequestration of calcium triggered by osteoblastic bone activity that leads to hyperparathyroidism in response to increased calcium demand. This case illustrates the importance of recognizing metastatic prostate malignancy as a potential culprit for hungry bone syndrome. Treatment usually will require high doses of calcium and calcitriol replacement as this hypocalcemia can be persistent with a high risk for mortality. Presentation: Saturday, July 12, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.571
Primary Topic
Parathyroid Disorders and Treatments
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article
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article

SAT-714 Bone Appétit: A Case Of Hungry Bone Syndrome In Prostate Cancer

Carolina Quintana-Ocasio, Miguel Santos-Lopez, Norma Vergne-Santiago, Gisela Feliciano-Diaz
Journal of the Endocrine Society
Parathyroid Disorders and Treatments
article

SAT-714 Bone Appétit: A Case Of Hungry Bone Syndrome In Prostate Cancer

Carolina Quintana-Ocasio, Miguel Santos-Lopez, Norma Vergne-Santiago, Gisela Feliciano-Diaz
article en

Abstract

Abstract Disclosure: C. Quintana-Ocasio: None. M. Santos-Lopez: None. N. Vergne-Santiago: None. G. Feliciano-Diaz: None. Hungry bone syndrome is a well recognized metabolic disease characterized by excessive calcium and phosphorus sequestration in the bone, manifesting as hypocalcemia and hypophosphatemia. It is most commonly seen as a complication of parathyroidectomy in patients with long standing primary hyperparathyroidism. Prostate cancer is the most common cancer among males in the US and its the second-leading cause of cancer-related death. Hungry bone syndrome can be a rare complication of metastatic prostate malignancy but its exact incidence is not clearly established in the medical literature. An 80-year-old male with a complex medical history consisting of metastatic prostate cancer on active chemotherapy and chronic kidney disease (CKD) who was admitted to the hospital with complicated urinary tract infection. He exhibited symptoms of fatigue, perioral numbness, and muscle cramps. Case was complicated after developing a generalized tonic-clonic seizure requiring endotracheal intubation. Further work up revealed persistent hypocalcemia. Electrocardiogram presented a prolonged QT interval. Laboratory evaluation demonstrated severe hypocalcemia (corrected non-ionized calcium 3.4 mg/dL) and low ionized calcium (3 mg/dL [4.5 - 5.6 mg/dL]), elevated alkaline phosphatase 353 u/L [46 - 116 u/L], with elevated parathyroid hormone levels 446 pg/dL [18.5 - 88 pg/dL]. Extensive osteoblastic bone metastases were confirmed on imaging. During hospitalization, hypocalcemia was refractory necessitating multiple intravenous calcium infusion, calcitriol and cholecalciferol. He was discharged on calcium carbonate 600 mg 2 tablets TID, calcitriol 2 mcg BID and an extra 1000 mg of elemental calcium at bedtime. Hypocalcemia in the context of metastatic prostate cancer can be explained by increased sequestration of calcium triggered by osteoblastic bone activity that leads to hyperparathyroidism in response to increased calcium demand. This case illustrates the importance of recognizing metastatic prostate malignancy as a potential culprit for hungry bone syndrome. Treatment usually will require high doses of calcium and calcitriol replacement as this hypocalcemia can be persistent with a high risk for mortality. Presentation: Saturday, July 12, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Hospital Episcopal San Lucas (PR)
Openalex Percentile: Top 66%
Parathyroid Disorders and Treatments
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