^3rd Global Experts Meeting on Medical Case Reports May 09-10, 2016 New Orleans, Louisiana, USA

Sowmya Nanjappa has received her MD degree from Bangalore Medical College in India. She has completed an Internal Medicine Residency at Wyckoff Heights Medical Center (affiliated to Cornell Presbyterian), New York. She has recently completed a Fellowship in Infectious Diseases at Saint Louis University School of Medicine. Her clinical interests are in treatment of infectious diseases and antibiotic stewardship and her research focus is in infectious diseases in oncology patients.

Introduction: Hypercalcemia in metastatic breast cancer is generally secondary to bone metastases. In a few cases, hypercalcemia secondary to secretion of parathyroid hormone related protein (PTHrP) is reported in squamous cell tumors, known as humoral hypercalcemia of malignancy. Ectopic tumor secretion of PTH or vitamin D resulting in hypercalcemia is seen in rare cases. rnCase: A 67 year old woman presented with metastatic poorly differentiated breast carcinoma with neuroendocrine differentiation to the right axillary lymph nodes. She underwent 6 cycles of cyclophosphamide/adriamycin and was placed on hormonal therapy. Four years after diagnosis, she developed metastatic disease in her liver and was treated with 3 cycles of carboplatin/taxol. Since she had minimal response and liver predominant disease, she was treated with radio embolization to the right and left lobes followed by Xeloda. She presented with lethargy and generalized weakness during subsequent clinic visits. Serial labs demonstrated progressive hypercalcemia with serum calcium levels between 12-16 meq/ml. She was treated with IV fluids and bisphosphonates, resulting in temporary improvement. Further evaluation showed elevated PTHrp with low intact PTH. rnDiscussion: Published literature exists regarding TAE treatment of hypercalcemia of malignancy secondary to HCC. However, this is the first case report where hepatic artery TAE was successfully used to treat paraneoplastic hypercalcemia secondary to metastatic breast cancer. TAE has been established as the primary therapy when hypercalcemia of HCC is caused by tumor secretion of humoral mediators signaling calcium release from bone rather than hypercalcemia secondary to bone metastasis. A similar type of pathway could explain the hypercalcemia seen here. Ours is the first case, demonstrating that the use of TAE in patients with refractory hypercalcemia secondary to paraneoplastic syndrome of metastatic breast cancer is an effective treatment option.