(12.03) A Rare Case of Decompensated Liver Cirrhosis- Induced Hypercalcemia

Introduction : Cirrhosis-induced hypercalcemia is rare and poorly understood, and should only be diagnosed after excluding all common causes of hypercalcemia. We present a patient who developed idiopathic hypercalcemia associated with increasing bilirubin levels and decompensated NASH- cirrhosis, with extensive workup performed to exclude other causes of hypercalcemia.

Case(s) Description : A 65-year-old male with past medical history of suspected NASH-induced decompensated liver cirrhosis was transferred from an outside hospital for evaluation for a liver transplant. Hospital admission was complicated by spontaneous bacterial peritonitis treated with antibiotics, portal vein thromboses, ascites status post multiple paracentesis, newfound coronary artery disease making patient no longer a candidate for transplant. On physical examination, the patient had severe abdominal distension, jaundiced skin with icterus, but was not encephalopathic. Labs revealed elevated liver enzymes that continued to worsen, and a bilirubin level that peaked at 9.9. Patient also subsequently developed new onset hypercalcemia, with calcium levels peaking at 11.1. Extensive workup for hypercalcemia was ordered. Intact PTH, PTH related protein, and AFP were within normal limits, excluding parathyroid or malignancy related causes of hypercalcemia. Vitamin D levels were low, ruling out Vitamin D toxicity. TSH levels were normal, and a thyroid ultrasound was unrevealing, ruling out thyroid related causes as well. Patient developed suspected contrast- induced nephropathy throughout the admission, but calcium levels were still elevated even after patient’s kidney function improved. A 24- hour urine calcium was unable to be performed due to the patient being on diuretics. There was no family history of familial hypocalciuric hypercalcemia and prior to hospitalization, the patient did not have any restricted mobility or periods of prolonged immobilization. After excluding the usual causes of hypercalcemia, it was presumed that the hypercalcemia was secondary to patient’s decompensated liver disease.

Discussion : The pathogenesis of cirrhosis-induced hypercalcemia is poorly studied and not well understood. It is hypothesized that acute decompensation of cirrhosis can lead to an increased inflammatory state, resulting in inflammatory mediators being released causing bone resorption and consequent hypercalcemia. Therefore, hypercalcemia in cirrhosis should be a diagnosis of exclusion and rigorous workup of other causes of hypercalcemia should be thoroughly explored first.