Journal Article

SUN-786 Idiopathic Hypercalcemia of Liver Cirrhosis

Chandran, Shaeker, Perez, Julienne Sanchez, Bedell, Brandon Robert

2025

Overview

Abstract Disclosure: S. Chandran: None. B.R. Bedell: None. J. Sanchez Perez: None. Background: Fewer than 20 case reports have described idiopathic hypercalcemia in patients with advanced cirrhosis (1). In these cases, no other predominant mechanisms for PTH-independent hypercalcemia were identified, representing a rare and poorly understood phenomenon in chronic liver disease. We present a case of idiopathic hypercalcemia in a patient with advanced decompensated cirrhosis and discuss a proposed underlying mechanism. Clinical Case A 52-year-old male with a history of alcohol-associated cirrhosis presented with altered mental status. On physical examination, he exhibited jaundice, significant ascites and asterixis. Labs revealed hypernatremia, elevated bilirubin, acute kidney injury with a creatinine of 2.2 mg/dL (reference range: 0.5-1.5 mg/dL) from a baseline of 1 mg/dL, and hypercalcemia with a calcium of 11.1 mg/dL (8.6-10.6 mg/dL) and an ionized calcium of 6.7 mg/dL (4.2-5.4 mg/dL). Work-up was notable for a parathyroid hormone (PTH) level of 11 pg/mL (12-88 pg/mL), suggesting a PTH-independent process. Further testing for hypercalcemia etiology was also non-revealing: TSH was of 0.73 mciu/mL (0.35-4 mciu/mL), PTHrP was undetectable, 25 OH Vit D was 8 ng/mL (20-80 ng/mL), 1,25-dihydroxy Vit D was 7.0 pg/mL (19.9-79.3 pg/mL), and Vitamin A was 0.08 mg/L (0.3-1.2 mg/L). There was no history of use of thiazides, lithium, or antacids. Imaging did not reveal any focal hepatic lesions. The patient was initially treated with intravenous hydration (normal saline) and calcitonin (4 units/kg BID for five doses), resulting in temporary resolution of hypercalcemia. However, hypercalcemia recurred five days later with an ionized calcium level of 6.5 mg/dL. A dose of Zolendronic Acid (4mg) was administered. Despite this, the patient’s clinical condition deteriorated, and family elected to pursue hospice care. Conclusion: Given the exclusion of typical causes of hypercalcemia, we conclude that the patient’s hypercalcemia may represent idiopathic hypercalcemia of liver cirrhosis. This is a rare phenomenon which adds to the existing literature. The recurrence of hypercalcemia despite treatment raises questions about the underlying pathophysiology and the role of bisphosphonates in this population. Additionally, an elevated C-telopeptide (1275 pm/mL, reference range: 161-737 pm/mL) in our patient suggests that increased bone turnover, potentially driven by cytokine-induced inflammation in acute decompensated cirrhosis (2), may have contributed to the hypercalcemia. References: 1.Zulfikar, Rafia MD; Silodia, Alok MD. Hypercalcemia in Chronic Liver Disease: A Rare Entity: 1207. American Journal of Gastroenterology 108():p S354, October 2013.2.Cadranel, J. F., Cadranel, J., Buffet, C., Ink, O., Pelletier, G., Bismuth, E., & Etienne, J. P. (1989). Hypercalcaemia associated with chronic viral hepatitis. Postgraduate Medical Journal, 65(767), 678-680. Presentation: Sunday, July 13, 2025

• Publisher: Oxford University Press
• Subject: Hypercalcemia / Liver cirrhosis / Liver diseases