Idiopathic Hypercalcemia Secondary to Hyperbilirubinemia in the Setting of Acute Liver Failure
Document Type
Conference Proceeding - Restricted Access
Publication Date
5-9-2025
Abstract
Altered mental status can result from a wide range of causes, including metabolic disturbances, organ dysfunction, medications, and psychiatric conditions. Hypercalcemia is a known cause of altered mental status, often resulting from conditions such as primary hyperparathyroidism or malignancy. However, hypercalcemia associated with liver dysfunction, particularly in the context of hyperbilirubinemia, is not well understood. Although liver disease has been linked to disruptions in calcium metabolism, the exact pathophysiological mechanisms remain unclear. This case presents an example of altered mental status correlated with idiopathic hypercalcemia secondary to hyperbilirubinemia.
A 36-year-old male with a history of non-ischemic cardiomyopathy with recovered ejection fraction, opioid use disorder on methadone therapy, and hypertension presented with progressive jaundice, fatigue, hypotension, and altered mental status. On examination, the patient was lethargic but arousable, able to answer questions before returning to sleep. Abdominal examination revealed hepatomegaly, and dermatologic examination showed diffuse jaundice with scleral icterus. Laboratory findings included a creatinine of 5.0 mg/dL, BUN of 126 mg/dL, elevated bilirubin of 50.6 mg/dL, normal AST (27 U/L) and ALT (23 U/L), and elevated ammonia of 122 µg/dL. Initial calcium was normal at 10.2 mg/dL, with a serum albumin of 3.6 g/dL. Initial workup, including viral hepatitis panel, acetaminophen and ethanol levels, toxicology screening, liver ultrasound, TTE, and MRCP, was unremarkable, excluding conditions like acute cholangitis and congestive hepatopathy.
Further evaluation of acute renal failure revealed no obstructive uropathy on renal ultrasound or abdominal CT. Serum and urine studies indicated acute tubular necrosis. Blood cultures were unremarkable. After stabilization, bilirubin, creatinine, and BUN decreased, but mental status did not improve. Head imaging was negative. Lactulose/rifaximin treatment was ineffective. Psychiatry ruled out methadone over-sedation. Serum calcium gradually increased from 10.2 mg/dL to 12.9 mg/dL, with endocrinology confirming parathyroid hormone-independent hypercalcemia. Further workup for sarcoidosis, malignancy, and PTHrP was negative, leading to a diagnosis of idiopathic hypercalcemia. The patient was treated with intravenous fluids, improving renal function, though bilirubin and calcium levels remained stagnant. At outpatient follow-up, mental status had returned to baseline, and lab work showed resolution of kidney injury and normalization of bilirubin and calcium.
The patient's mental status improved with physiologic bilirubin clearance. Notably, the resolution of hypercalcemia and return of cognitive function paralleled the decline in bilirubin levels. The relationship between calcium and bilirubin homeostasis remains poorly understood, and further research is needed to explore this potential link and refine diagnostic approaches for similar cases. This highlights the necessity for clinicians to consider idiopathic hypercalcemia as a possible cause when managing patients with hyperbilirubinemia and altered mental status.
Recommended Citation
Sabbaq R, Mohiddin O, Mohiddin T, Bdeir S, Sclair S. Idiopathic hypercalcemia secondary to hyperbilirubinemia in the setting of acute liver failure. Presented at: Research Day Corewell Health West; 2025 May 9; Grand Rapids, MI.
Comments
2025 Research Day Corewell Health West, Grand Rapids, MI, May 9, 2025. Abstract 1840