NIV 2014

Introduction: Hypocalcemia is a relatively common finding in patients with active malignancy and is mostly mild and asymptomatic. In most cases hypocalcemia is the result of hypoalbuminemia, vitamin D deficiency, bisphononate use, tumor lysis syndrome or treatment with chemotherapy. Another cause of hypocalcemia may be calcium utilisation by extensive osteoblastic metastases, mostly seen in prostate cancer or breast cancer. Severe or life-threatening hypocalcemia however is uncommon. We present a case of severe hypocalcemia due to osteoblastic metastases in prostate cancer.

Case: A 66-year old Caucasian man was referred for admission to the cardiology department with dyspnea, muscle weakness and paresthesia. His medical history included Crohn’s disease for which an ileocecal resection was performed in 2007 due to complicated fistulae. On admission, the patient was confused and not able to walk. Trousseau’s sign was positive. Chest X-ray showed signs of pulmonary edema. Electrocardiography showed a prolonged QT interval (504 ms) and inverted T waves in leads II, III and aVF. Echocardiography was performed subsequently and showed a severe dilating cardiomyopathy and mitral valve regurgitation with a poor left ventricular function. Laboratory investigation showed a total calcium value of 0,91 mmol/L with a normal serum albumin and a serum magnesium value of 0,20 mmol/L. Initially gastrointestinal malabsorption was interpreted as the cause of the electrolyte disturbances and intravenous supplementation of calcium and magnesium was started. Raising electrolyte levels proved to be difficult however. Further laboratory tests showed an alkaline phosphatase value of 534 U/L, indicating increased bone turnover. A bone scintigraphy was performed and was evaluated as a so called ‘superscan’ an intense symmetric activity in the bones with diminished renal activity, highly suspicious for diffuse metastatic disease. Prostate cancer was suspected and the prostate-specific antigen (PSA) level was 3370 µg/L. Prostate biopsy showed adenocarcinoma, Gleason 4+3 and treatment with leuprorelin and bicalutamide was initiated. After prolonged intravenous supplementation of calcium and magnesium, serum values started to normalize. Subsequent echocardiography showed significant improvement of the left ventricular function. Calcium and magnesium values eventually remained stable under oral supplementation.

Conclusion: This case illustrates that severe symptomatic hypocalcemia and hypomagnesemia can occur in association with extensive osteoblastic metastases in prostate cancer. Calcium and in lesser extent magnesium, are consumed in large amounts through new metastatic bone formation, the so-called hungry bone syndrome. Hypocalcemia-induced dilating cardiomyopathy improved after calcium supplementation. In conclusion, clinicians should be aware of osteoblastic metastases as a cause of severe hypocalcemia.