NIV Congres

Introduction: Prostate carcinoma is a common malignancy which often metastasizes to the bone. Although bone metastases from prostate cancer have a primary osteoblastic nature, a significant osteoclastic component exists. Excess osteoclastic activity can lead to bone destruction, causing skeletal related events defined as bone pain, pathologic fractures and spinal cord compression. Bisphosphonates are currently used to reduce these complications. We report a case of prolonged hypocalcemia due to the use of pamidronic acid.

Case: A 74 year old man was seen at the emergency room with nausea and dysphagia. His medical history included a castrate resistant prostate carcinoma with bone metastases. He was currently treated with cabazitaxel, prednisone and pamidronic acid on a monthly schedule. Physical examination and an ECG revealed no abnormalities. Initial laboratory investigations showed a hypocalcaemia of 1.61 mmol/L and a hypophosphatemia of 0.2 mmol/L. Further investigations showed an elevated parathyroid hormone level of 13 pmol/L (2-7) and a mild vitamin D deficiency of 28 nmol/L (50-200). Review of the past laboratory values showed a declining calcium level and no prior assessment of vitamin D levels. A fractional phosphate excretion of 15% revealed phosphate was actively excreted, most likely because of the hyperparathyroidism. Urine calcium was low (<1.3 mmol/L), suggesting compensatory renal calcium absorption. It is well known bisphosphonates have an inhibitory effect on the function of the osteoclast, preventing bone resorption. Previous research hypothesized that bisphosphonates also possess a stimulating effect on osteoblasts causing an avid calcium uptake in bone, resulting in hypocalcemia. We believe this mechanism may have caused the prolonged calcium and phosphate imbalance in our patient. Secondary a mild vitamin D deficiency prevented a compensatory response. Our patient was admitted for 19 days. He received a high dose of oral and intravenous calcium and phosphate supplements. Vitamin D and activated vitamin D were added. Pamidronic acid was discontinued. After 110 days his calcium and phosphate levels normalized.

Conclusion: We described a patient with prolonged hypocalcemia and hypophosphatemia due to the use of pamidronic acid and a mild vitamin D deficiency. Current opinion states that calcium and vitamin D levels have to be checked and corrected prior to start of bisphosphonates. But as this case shows, it is also important that calcium and vitamin D are checked on a regular basis during the use of bisphosponates. Furthermore, prophylactic suppletion of calcium and vitamin D, if no contra-indications are present, is advised.