Endocrine Abstracts

Introduction: Brown tumours (BT) are a recognised complication of severe prolonged untreated hyperparathyroidism (HPT). BT can mimic bone metastases and giant cell tumors (GCT). Hungry bone syndrome (HBS) is a severe and prolonged, postoperative hypocalcemia following parathyroidectomy. BT are a risk factor for HBS. We report the case of a young lady with BT masquerading as a GCT, from a tertiary centre in India.

Case study: A 25 year lady presented with pathological fractures of humerus, tibia and inabilty to weight bear. MRI in primary care, showed multiple hyperintense (T2 imaging) expansile lytic lesions over humerus, pelvis and femur with compression fracture of vertebrae. FNAC was suggestive of giant cell tumour. PET-CT confirmed hypermetabolic multifocal expansile bone lesions with fractures and osteoporotic vertebrae with no evidence of primary malignancy, raising a differential diagnosis of brown tumours. Biochemistry revealed elevated calcium (S.Ca 11.9 mg/dl, normal range (NR) 8.8–10.6), Alkaline phosphatase(304 IU/L,(NR 53–141)). Parathyroid hormone(PTH) was elevated: PTH 486 pg/ml (NR 10.0 −65 pg/ml) with severe Vitamin D deficiency: 6.5 ng/ml(NR 30–100 ng/ml), low phosphorous 1.7 mg/dl(NR 2.5–4.5 mg/dl). A diagnosis of primary HPT with brown tumours was made.PETCT, contrast enhanced CT and targeted ultrasound failed to localize a parathyroid adenoma. Sestamibi scan showed faint uptake at the right superior parathyroid. Preoperatively a loading dose of 300,000 units of Intramuscular and 200 units of oral cholecalciferol was given. Consent for targeted parathyroidectomy and possible full neck exploration was taken. Right superior parathyroid gland of 1.6×1.2 cm was excised, which was thin and flat (probably the reason for missing on CT/ultrasound). Significant decrease in intraoperative PTH level (628.1–35.5 pg/ml) was observed. Intra-operative frozen section confirmed parathyroid adenoma.Post procedure she developed HBS (mean calcium 7.9 mg/dl) remaining asymptomatic. She required escalating dose of oral calcium upto 15 g of elemental calcium and 4 mg calcitriol with intermittent intravenous calcium and magnesium supplements. Proton pump inhibitors (PPI) were with-held. Post discharge calcium remained stable around 9 mg/dl with above dose of calcium and calcitriol. Pathological fractures are being managed conservatively.

Conclusion: BT is an important differential diagnosis for lytic expansile bone lesions with giant cell morphology on histology. BT often resolves with HPT treatment. Early diagnosis aviods complex surgical intervention.BT increases risk of post-operative HBS. Pre-operative loading of Vitamin D may have reduced duration and severity of HBS. However more evidence is needed to support this approach. Correction of Hypomagnesemia and withholding PPI aids optimal absorption of oral calcium.