Abstract Introduction Calcium is a mineral that is required for nearly every cell in the human body to operate properly. Calcium homeostasis is mediated by active vitamin D (calcitriol) and parathyroid hormone (PTH) on calcium absorption in the GI tract, calcium excretion in the kidney, and osteoclast/osteoblast activity in the skeleton. Under normal settings, PTH promotes bone production and resorption by increasing the number of osteoblasts and, as a result, indirectly increasing the number of osteoclasts. Hypocalcemia, a decrease in extracellular calcium defined as serum total calcium < 8.5 mg/dl corrected for serum albumin. Hypocalcemia is caused by a lack of vitamin D (which can lead to secondary hyperparathyroidism), abnormal phosphate or magnesium levels, and partial or complete hypoparathyroidism. Hypocalcemia was found to be present in 1.6% of cases of cancer. We present a patient with prostate cancer and severe hypocalcemia, predominantly due to extensive osteoblastic metastases. Clinical case: A 42 y/o Male with prostate cancer metastases to bone and lymph Nodes developed severe hypocalcemia and hypophosphatemia during the course of treatment. Patient was treated aggressively with per oral (PO) and intravenous (IV) calcium and phosphorous supplementation with no significant improvement in the values. Vitals were stable except for a heart rate of 101 beats per minute. The physical exam was normal. Labs: Calcium-5.1 mg/dl(8.5-10.1), Ionized calcium-0.74 mmol/L(1.2-1.38), Albumin-4.2gm/dl(3.4-5. 0),Phosphorous - 0.6 mg/dl(2.5-4.9), Alkaline phosphatase- 1.573 units/l(45-117), Magnesium-1.8mg/dl(1.7-2.4), Vitamin D25 OH-17ng/ml(30-100), PTH-281 pg/ml(18.4-88), Ferritin-725ng/ml(30-300), TSH- 1.45 ulU/ml(0.36-3.74). Imaging: CT scan chest/abdomen/pelvis showed metastatic disease throughout sternum, lumbar spine, pelvis, and proximal femur. MRI thoracic spine showed extensive metastatic disease throughout the thoracic spine. The patient was diagnosed with hypocalcemia in the setting of metastatic prostate cancer due to avid calcium uptake by bone metastasis. The patient was treated with radiation therapy, high dose Vitamin D every week, calcitriol, phosphorous, and labs were closely monitored every month. His labs showed normalized calcium, phosphorous, alkaline phosphatase, and Vitamin D level after eleven months, and his symptoms improved. This improvement was paralleled by a significant improvement in PSA concentrations while on androgen deprivation therapy and chemotherapy for Prostate cancer. Conclusion Hypocalcemia in cancer patients is a rare event. However, it can be life-threatening, so it is essential to rule out other causes by measuring magnesium, creatinine, phosphate, vitamin D, and PTH levels to determine the treatment. Hypocalcemia can occur at any time during therapy, it is most frequently reported within six months of treatment initiation. For patients with a substantial burden in bone (=>three bone lesions), prophylactic calcium and vitamin D are associated with fewer hypocalcemia adverse effects. Patients should be informed about the risk of hypocalcemia and the significance of supplement adherence, serum calcium levels should be checked to assess adherence with close follow-up. Presentation: No date and time listed
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