Severe Bisphosphonate Induced Hypocalcaemia in the Background of Severe Necrotizing Pancreatitis due to Primary Hyperparathyroidism.

Abstract

Bisphosphonates are pyrophosphate analogues that bind at the bone mineral surface, where they potently inhibit osteoclast-mediated bone resorption. They are used in the treatment of hypercalcemia due to malignancy, osteolytic lesions from multiple myeloma, bone metastasis from solid tumours, osteoporosis, and Paget’s disease. They have also been used effectively in the medical management of primary hyperparathyroidism to decrease serum calcium.1,2 Inhibition of osteoclast activity in bone by bisphosphonates can result in hypocalcaemia and hypophosphatemia. The majority of patients do not manifest hypocalcaemia due to compensatory mechanisms such as raised Parathyroid Hormone (PTH). However, in patients with low Vitamin D levels, renal failure, prior parathyroidectomy, hypomagnesemia, and hypoparathyroidism, these compensatory mechanisms may be blocked, resulting in hypocalcaemia.3-5 Here we report a case in which the use of bisphosphonate for severe hypercalcemia due to primary hyperparathyroidism, led to life-threatening hypocalcaemia. Case Report