ODP084 Denosumab as a therapuetic modality in management of primary hyperparathyroidism induced severe hypercalcemia

Abstract

Abstract Background Primary Hyperparathyroidism(due to parathyroid adenoma) is usually associated with smoldering clinical course due to effects of chronic hypercalcemia whereas malignancy related hypercalcemia is often associated with life threatening severe hypercalcemia. However in rare instances, hypercalcemic crisis may be sole presenting feature of primary hyperparathyroidism. The role and utility of denosumab therapy in such clinical settings is less well studied. Case Report: A 53 year old male patient was referred for evaluation of severe hypercalcemia. He presented with symptoms of nausea, vomiting and constipation for last two weeks. He did not give any history of abdominal pain, polyuria, polydipsia, nephrolithiasis, bony fractures, acid peptic disease or cognitive impairment in past. He was a known case of type 2 diabetes mellitus for last 2 years and was on oral anti diabetic drugs with fairly good glycemic control. On evaluation, the patient was conscious, oriented and lethargic. His vitals were stable and systemic examination was grossly normal. Abdominal imaging including upper gastrointestinal endoscopy for his above complaints revealed no gross abnormality. Significant positive findings from biochemical evaluation included: severe hypercalcemia(serum calcium level-20.45 mg/dl, normal: 8.6-10.3mg/dl), serum phosphorous-2. 09mg/dl(normal: 2.7-4.5mg/dl), serum albumin-4.26g/dl(normal: 3.4-4.4g/dl) and serum creatinine-3.1mg/dl(normal: 0.8-1.5mg/dl). A kidney function test done during periodic health screening two months ago was absolutely normal(serum creatinine: 0.9 mg/dl). PTH levels were found to be significantly elevated (1383.6pg/ml, normal: 15-65pg/ml). A presumptive diagnosis of primary hyperparathyroidism induced severe hypercalcemia with acute kidney injury was made. He was initially managed with saline rehydration followed by diuretic therapy and subcutaneous calcitonin administration. However, no significant response was seen. In view of his deteriorating renal function and severe hypercalcemia, immediate hemodialysis was planned in consultation with nephrologist. Despite three sessions of hemodialysis, his serum calcium and creatinine levels were lowered to 17.69mg/dl and 2.1mg/dl respectively. Owing to refractory and persistent hypercalcemia, injection denosumab(60 mg sc) was subsequently administered. Following denoumab therapy, serum calcium continued to show a declining trend and it came down to 10.8mg/dl by end of fourth day. In the meantime, localization studies including neck ultrasonography and Technetium 99m sestamibi scan confirmed presence of right inferior parathyroid adenoma. The patient subsequently underwent successful focused parathyroidectomy with rapid improvement in his health status. Following surgery, he was managed with calcium and calcitriol supplementation to maintain normocalcemia. Histopathological examination of excised tumor confirmed presence of parathyroid adenoma. Conclusion Hypercalcemic crisis can be a rare presenting feature of primary hyperparathyroidism. Denosumab therapy can play a pivotal role in managing such patients(especially when other therapeutic modalities fail to control underlying severe hypercalcemic state) and act as beneficial bridging therapy till definitive surgery can be undertaken. Presentation: No date and time listed