Nicardipine-induced acute hepatitis in an intensive care unit patient.

Drug-related hepatotoxicity is now the leading cause of acute liver failure in the United States, especially among patients who have no prior liver disease. Nicardipine is the only IV calcium channel blocker available for the short-term treatment of hypertension with a considerably good safety profile. We report a case of nicardipine-induced hepatitis. A patient with history of hypertension was admitted because of right middle cerebral artery infarction. Computed tomography of the brain showed evolving stroke. The patient went for cerebral angiography and stent placement, and during the procedure he had cerebral hemorrhage. He was transferred to neurosurgery. After surgery, he was started on hypertonic saline, mannitol for cerebral edema, and nicardipine drip for blood pressure control. On the fourth day after operation, he started to have fever with progressive elevation of liver enzymes [Aspartate amino transferase (AST) 450, Alanine amino transferase (ALT) 356, and alkaline phosphatase 299]. Serum bilirubin was 0.6. He did not receive blood transfusion. No medical history of hepatitis or liver disease was reported. Other medications included metoprolol and heparin. White blood cell count was 13,000. Chest x-ray did not show evidence of consolidation. Urine analysis was unremarkable. Cultures were negative. Acute hepatitis panel was negative. Cerebrospinal fluid examination was normal. Liver enzymes were trending up gradually with normal protein and bilirubin. Computed tomography of the abdomen was unremarkable. The patient's medications were reviewed. It was noticed that the patient started to have fever and elevated liver enzymes after administration of nicardipine drip. It was postulated that nicardipine may be the culprit of acute hepatitis. Nicardipine drip was stopped, and the patient was started on labetalol. Fever started to resolve, and liver enzymes started trending down toward normal. The patient remained afebrile after that.