SAT-492 Intact PTH Secretion from Hepatocellular Carcinoma in a Patient Presenting with Hypercalcemia

Abstract

Background Hypercalcemia of malignancy is typically associated with bony metastases or production of PTHrP. However, rarely, it can be due to intact PTH (iPTH) secretion from solid tumors1. Clinical Case A 61 year old man with chronic kidney disease and hepatitis C cirrhosis complicated by hepatocellular carcinoma (HCC) presented with abdominal pain and was found to have hypercalcemia and a new 5 cm mesenteric mass. Admission labs showed PTH-mediated hypercalcemia: calcium 12.7 mg/dl (8.5-10.1 mg/dl), albumin 3.1 g/dl (3.5-4.8 g/dl), serum creatinine 2.4 mg/dl (0.6-1.4 mg/dl), PTH 397.4 pg/ml (18.4-88 pg/ml), PTHrP 16 (14-27 pg/ml), 25-OH Vitamin D 12.9 ng/ml (30-100 ng/dl), and 1,25-OH Vitamin D 12 (18-72 pg/ml). SPEP and UPEP were normal. Prior to presentation, his baseline calcium was normal and PTH had ranged 150-180 pg/ml with similar renal function as on admission. A parathyroid ultrasound and sestamibi scan were negative for a parathyroid adenoma. A nuclear bone scan was negative for bony metastases. An octreotide scan was also negative. A PET-CT scan showed an FDG-avid mesenteric mass and new FDG-avid hepatic lesions. A biopsy of the mesenteric mass was consistent with metastatic HCC and stained positive for PTH, which suggested iPTH secretion from the HCC. The patient was given IV fluid, calcitonin and cinacalcet with minimal improvement in his hypercalcemia. He later received pamidronte and also underwent embolization to one of the larger hepatic HCC lesions. The mesenteric HCC lesion was not resectable, nor was it amendable to embolization. His calcium normalized after treatment, though his PTH remained very elevated, indicating this improvement was from the pamidronate and not the embolization. Hypercalcemia in other reported cases of iPTH secretion from HCC did improve after embolization2,3, though in these cases, the HCC had not metastasized. The patient had several recurrent admissions for hypercalcemia with increasingly poor response to bisphosphonates. His PTH had climbed to 1275 pg/ml. Denosumab therapy was considered, but he had transitioned to hospice care and died 3 months after his initial presentation. Conclusion Intact PTH secretion from HCC is a rare cause of hypercalcemia