Endocrine Abstracts

In May 2011 a 55-year-old South East Asian man had a tumour removed from the floor of his mouth. The histology was consistent with a brown tumour of hyperparathyroidism. His PTH was raised at 12.3 pmol/l (NR 1.6–7.5) and he was referred to the endocrinology clinic. His serum calcium was 2.22 mmol/l (NR 2.2–2.6 mmol/l) and his serum 25 (OH) vitamin D level was <15 (NR >50 nmol/l) with a normal alkaline phosphatase. He had no symptoms of osteomalacia. He is a vegetarian. His past medical history included hypertension, hyperlipidaemia and a pulmonary embolism in 2005. His results were consistent with secondary hyperparathyroidism due to severe vitamin D deficiency. He was given replacement therapy and when discharged from the clinic in November 2011 his PTH was normal at 3.8 pmol/l, his serum calcium was 2.35 mmo/l and his vitamin D level was 165 nmol/l. He was advised to take 25 μg (1000 IU) of colecalciferol lifelong. In March/April 2012 the patient noticed swelling in the right maxilla which progressively got bigger. A CT scan of the lesion showed an expansile lesion in the right maxillary alveolus. Biopsy again showed features consistent with a brown tumour of hyperparathyroidism. His repeat PTH was normal at 3.9 pmol/l with a normal serum calcium of 2.34 mmol/l and his serum 25 (OH) vitamin D level was 48 nmol/l. His urinary calcium excretion was normal (5.9 mmol/24 h – NR 2.5–7.5). He was advised to increase his colecalciferol to 50 μg (2000 IU) per day. An ultrasound scan of his parathyroid glands was essentially normal.

Brown tumours are non-neoplastic lesions resulting from abnormal bone metabolism and are known to be associated with primary hyperparathyroidism. There have been case reports of peripheral brown tumour in the maxilla as manifestation of secondary hyperparathyroidism associated with chronic renal failure but to our knowledge there have been no reports of a brown tumour due to secondary hyperparathyroidism as a result of severe vitamin D deficiency. Furthermore it is unclear why the patient developed a further brown tumour after his secondary hyperparathyroidism had been corrected.