Endocrine Abstracts

A 56 year old lady was diagnosed with cancer of unknown primary after the discovery of liver metastases. Prior to the commencement of EOX chemotherapy (epirubicin, oxaliplatin and capecitabine) she was given a dose of 4 mg zolendronic acid for hypercalcaemia of malignancy. Three weeks later she presented to our hospital with a history of rapid decline and reduced oral intake, with associated diarrhoea. She had reduced GCS and hypotension. Initial investigations revealed an acute kidney injury (Ur 74.4 mmol/l, Cr 461 umol/l) with normal potassium, severe hypocalcaemia at 1.10 mmol/l (adjusted) and magnesium 0.41 mmol/l (0.5–0.8). Electrocardiogram showed severe QTc prolongation at 587ms. She was managed on intensive care with intravenous antibiotics, fluids and electrolyte replacement. PTH was appropriately elevated at 32.8 pmol/l (1.5–7.6) with Vitamin D 27 nmol/l. Despite improving metabolic status her GCS remained persistently low; subsequent investigations revealed a normal MRI brain scan, lumbar puncture and paraneoplastic antibiotics. She was diagnosed with metabolic encephalopathy secondary to hypocalcaemia; over a period of four weeks she gradually improved with continued electrolyte correction. Hypercalcaemia of malignancy is found in up to 44% of patients with malignancy, with a number of potential mechanisms involved. Intravenous fluids and bisphosphonates remain amongst the mainstays of treatment. Hypocalcaemia is a recognised complication of zolendronate therapy, with trials suggesting up to 1% of patients may develop a significantly low calcium. The development of renal failure is both a potential complication of this treatment as well as a potentiator of it. Our case illustrates the rare occurrence of metabolic encephalopathy as a consequence of zolendronic acid treatment, risk factors of hypocalcaemia as well as highlighting the importance of giving appropriate education and arranging robust follow-up when patients treated with intravenous bisphosphonates are discharged.