Endocrine Abstracts

We report two cases of severe hypocalcaemia developed after intravenous administration of pamidronate in patients with severe hypercalcaemia secondary to multiple myeloma. Both of them develop symptomatic hypocalcaemia few days after treatment. Both patients was probably vitamin D deficient (both serum 25-hydroxyvitamin D level was low less than 15 (NR 25–120 nmol/l) because of a combination of poor oral intake, inadequate sunlight exposure, and the development of renal failure. However despite receiving both potential and oral calcium therapy, the serum calcium remained low until the replacement of vitamin D. Both patients had underlying conditions that impaired the homeostatic response to bisphosphonates and contributed to the severe hypocalcaemia. Review of published reports on symptomatic bisphosphonate-induced hypocalcaemia disclosed that hypocalcaemia develops in patients with unrecognized hypoparathyroidism, impaired renal function, or vitamin D deficiency. Overall, the rate of the development of hypocalcaemia was related to the potency of the bisphosphonate administered.

Conclusion: The increasing use of bisphosphonates and the introduction of more potent agents impose a considerable risk for bisphosphonate-induced hypocalcaemia in a substantial number of patients. Greater awareness of this complication, a better understanding of the underlying mechanisms, and proper assessment of patients in whom bisphosphonate therapy is contemplated should reduce the frequency of occurrence of hypocalcaemia.