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SUN-490 Enigmatic Presentations Of Hyperparathyroidism

Abstract Primary hyperparathyroidism is mostly due to an adenoma or hyperplasia of the parathyroid glands. Secondary hyperparathyroidism is mostly seen with renal failure and hypovitaminosis D. Skeletal complications of hyperparathyroidism are rare with better screening, and include osteitis fibrosa cystica, bone cysts and brown tumors; the later are composed of numerous multinucleated giant cells admixed with stromal cells and matrix, often seen in the jaw, long bones and ribs. Brown tumor as the first manifestation of hyperparathyroidism is quite rare; involvement of the spinal cord is even rarer with about 54 reported cases. Here we present 2 cases of brown tumors as the presenting manifestation of hyperparathyroidism. CASE 1: A 31 year old male with previous history of coronary artery disease, presented with swelling of right side of the jaw of 10 days duration.He reported history of altered behaviour, irritability, excessive fatigue and weight loss. On examination, he had a hard, nontender mandibular swelling with intraoral extension. Investigations showed severe hypercalcemia with corrected calcium of 19.4 mg/dl (8.6-10 mg/dl) and PTH intact (iPTH) of 1854 ng/ml (12-88 pg/ml). CT scan of the lesion showed large irregular lytic lesion of body and ramus of mandible on right side with a separate lesion in the right lower pole of thyroid s/o parathyroid adenoma and multiple lytic lesions in ribs and clavicles. He was managed with forced saline diuresis and haemofiltration for hypercalcemia; followed by parathyroidectomy with debulking of intraoral mass lesion. Intraop iPTH reduced to 408 ng/ml. Post operatively, he had hypocalcemia requiring correction. Histopathology of the parathyroid gland showed adenoma and the intraoral lesion was suggestive of brown tumor with osteoclasts and hemosiderin deposits. CASE 2: A 51 year old female with chronic kidney disease on maintenance hemodialysis for 3 years, presented with low backache and acute onset weakness of both lower limbs. Her iPTH was 673.1 pg/ml with S.Calcium of 7.7mg/dl. CT spine showed multiple lytic lesions involving C7, D3 and D11 vertebrae with cord compression at D11. MRI spine showed a well defined T1 hypointense and T2 hyperintense lesion measuring 2.4⨯3.6⨯2.7cms involving posterior elements of D11 vertebra, causing canal stenosis and cord compression. Ultrasound neck and sestamibi scans were negative for parathyroid adenoma. She underwent laminectomy with gross total excision of tumor. Histopathology of the lesion was suggestive of brown tumor. The diagnosis of secondary hyperparathyroidism with brown tumor of D11 vertebra causing paraparesis was made. She was commenced on Cinacalcet for hyperparathyroidism. CONCLUSION: We must exclude hyperparathyroidism as a cause in cases of lytic lesions of the bones. Both primary and secondary hyperparathyroidism should be kept in the differential diagnosis as the treatment will differ.