SUN-770 Severe Hypocalcemia in Diffuse Metastatic Prostate Cancer: Impact of Osteoblastic Lesions and Denosumab Therapy

Abstract Disclosure: G.I. Sydney: None. P. Balasubramanian: None. Background: Hypocalcemia in patients with metastatic prostate cancer is often multifactorial, with osteoblastic metastases playing a central role. Antiresorptive agents such as Denosumab are commonly used in the management of these cancers to decrease the incidence of skeletal related events and bone pain. However, these agents increase the risk of hypocalcemia which can be serious and life threatening if not promptly identified and treated. Clinical Case: We present a 71-year-old male with advanced prostate cancer and extensive osteoblastic metastases, admitted with bilateral subdural hematomas after a fall. He was treated with monthly Denosumab injections due to extensive skeletal metastases and received the last Denosumab dose one month prior to admission. Labs at time of admission revealed calcium of 6.2 mg/dL (reference range: 8.8 - 10.2 mg/dL), albumin 2.4 g/dL (reference range 3.6 - 4.9 g/dL; corrected calcium 7.5 mg/dL) iPTH 213 (reference range 15-65 pg/dL), magnesium 1.7 mg/dL (reference range 1.7 - 2.4 mg/dL), and creatinine 0.41 mg/dL (reference range 0.40 - 1.30 mg/dL). He endorsed fatigue and generalized weakness which he attributed to his cancer treatment but no other symptoms of hypocalcemia. Physical exam was significant for cachexia and Chvostek sign was negative. Vitamin D and 1, 25 vitamin D subsequently resulted as 52 ng/mL (reference range 20 - 50 ng/mL ) and 357 pg/dL (reference range 25-66 pg/dL). The hypocalcemia was attributed to a combination of osteoblastic metastases, recent Denosumab therapy, poor oral intake, and critical illness. He was managed aggressively, initially with a calcium gluconate drip and subsequently optimized on calcium citrate (1250 mg four times daily) and calcitriol (1 mcg BID) with concurrent magnesium repletion. His calcium and magnesium normalized within a few days and he was discharged with follow up. Conclusion: This case highlights the multifaceted etiology of hypocalcemia in metastatic prostate cancer, particularly in the presence of osteoblastic bone lesions and the use of antiresorptive therapy. Osteoblastic bone lesions promote calcium deposition and new bone formation resulting is decreased serum calcium levels. Parathyroid glands typically increase PTH secretion but are often ineffective at normalizing calcium levels despite severe secondary hyperparathyroidism. Antiresorptive agents increase the risk of hypocalcemia in these patients. Prompt identification and treatment with high doses of calcium, calcitriol and magnesium with close monitoring can prevent life threatening complications. Comprehensive evaluation of contributing factors and tailored therapeutic strategies are crucial to improving outcomes in this population. Presentation: Sunday, July 13, 2025