THU534 Humoral Hypercalcemia Of Malignancy As Initial Presentation Of Hepatocellular Carcinoma And Monoclonal Gammopathy Of Undetermined Significance

Abstract

Abstract Disclosure: F. Jovanovic: None. A. Raghavan: None. A. Sudhakar: None. Background: Humoral hypercalcemia of malignancy can be initial metabolic manifestation of different neoplasms, and it is exceedingly rare in hepatocellular carcinoma (HCC).1 In this case report, we present a patient with humoral hypercalcemia secondary to HCC and monoclonal gammopathy of undetermined significance (MGUS) in the context of nonalcoholic steatohepatitis. Case Report: A 73-year-old Caucasian male with liver cirrhosis secondary to nonalcoholic steatohepatitis presented to the emergency department with a two-week history of constipation and progressive confusion. The patient was jaundiced on exam and tender to palpation in left and right middle abdominal quadrants. Laboratory findings on admission showed serum calcium 12.7 mg/dL (7.9–10.6), albumin 2.6 g/dL (3.5–5), platelets 85x103/µL (138–338), alkaline phosphatase 349 unit/L (50–136), alanine aminotransferase 234 unit/L (15-53), aspartate aminotransferase 133 unit/L (15–37), alpha-fetoprotein 1912.7 ng/mL (0–8), parathyroid hormone <3 pg/mL (14–72), and ammonia 40 mmol/L (11–32). The patient’s altered mental status improved with lactulose and rifaximin. Serum calcium levels persisted despite lactated Ringer’s solution, but improved with zoledronic acid 5 mg infusion to a nadir of 9.1 mg/dL during the hospital stay. The patient was administered repeat zoledronic acid before discharge, but was readmitted 5 days later with worsening mental status and corrected serum calcium 13.1 mg/dL. The CT abdomen and pelvis showed a mass (4.2 x 3.7 cm) in the lower right hepatic lobe. The send out labs returned with PTH-related peptide 48 pg/mL (11–20), 1,25 hydroxyvitamin D 20 pg/mL (20–45), and serum protein electrophoresis with a monoclonal M spike 1.33 g/dL in the gamma globulin region. The patient’s hypercalcemia was found to be PTH–independent and with the new hepatic mass on CT imaging, he was diagnosed with MGUS and humoral hypercalcemia secondary to HCC. The literature review shows only one case report with alcoholic cirrhosis and similar clinical presentation, which is in contrast to nonalcoholic steatohepatitis as seen in our patient.2 The patient’s family refused further treatment and opted for hospice care. Conclusion: We recommend that the patients with HCC and resistant hypercalcemia undergo diagnostic evaluation for monoclonal paraprotein as part of humoral hypercalcemia workup.