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Bisphosphonates prevent the hungry bone syndrome.

Dr. A. Kumar, Department of Medicine and Therapeutics, University of Aberdeen, Polwarth Building, Foresterhill, Aberdeen AB9 2ZD, Scotland (UK) Sir, Bisphosphonates are a well-established treatment for hypercalcaemia of malignancy [1] and Paget’s disease of bone [2]. In recent years, bisphosphonates have also been used in the medical management of primary hy-perparathyroidism for temporary control of hypercalcaemia or in patients who are unwilling or unfit for parathyroid surgery [3]. An important complication of parathyroid-ectomy for severe primary hyperparathy-roidism is development of the ‘hungry bone syndrome’, which may cause severe, and sometimes lifethreatening hypocalcaemia, post-operatively [4]. Active metabolites of vitamin D have been given pre-operatively in an attempt to prevent this syndrome, with variable effects. Here we describe a patient with severe primary hyperparathyroidism who had bisphosphonate treatment for hypercalcaemia pre-operatively and who did not develop post-operative hypocalcaemia despite extensive parathyroid bone disease. A 62-year-old woman presented with a 6-month history of progressive lassitude, bone pain, intermittent nausea with accompanying abdominal pain, polyuria and mild confusion. She was found to be hypercal-caemic (serum adjusted calcium of 3.3 mmol/l; normal 2.1-2.6) and had a grossly elevated intact immunoreactive parathor-mone level (iPTH) of 1,271 ng/l (normal 10-65). Her urea was 22 mmol/l (2.5-6.5), creat-inine 215 μmol/l (60-110) and serum alkaline phosphatase 360 units/1 (45-105). Radiographs showed evidence of extensive hyperparathyroid-related bone disease in the hands, skull, spine and pelvis. Intravenous pamidronate 30 mg was given over 4 h, on 2 consecutive days. Prior to the second infusion her serum calcium had already fallen to 2.85 mmol/l and a nadir of 2.57 mmol/l was reached at 7 days. Satisfactory calcium levels were maintained without further intervention until she underwent parathyroidectomy 10 days later. The combined weight of the two parathyroid adenomata that were resected was 4.6 g. Post-operatively, serum calcium values were restored to normal; there was no acute hypocalcaemia, nor did she require calcium or vitamin D supplements. Serum calcidiol (2 5-hydroxy vitamin D3) and calcitriol (1,2 5dihydroxyvitamin D3) levels were measured prior to pamidronate treatment, and then at regular intervals before and after surgery over the next 3 weeks. The levels reflected chronic renal insufficiency. Calcidiol levels were normal between 15 and 25 nmol/l (reference range 15-100) and were not affected by treatment. The calcitriol level was 23 pmol/l (20-120) before treatment and was less than 15 pmol/l on all subsequent estimations. Between 13 and 30% of patients who undergo parathyroidectomy develop postoperative hypocalcaemia [4]. Clinical and biochemical features that appear to predict the occurrence of