Abstract

Introduction: Statins can cause an increase in liver enzymes, but these elevations resolve spontaneously in 70% of patients despite continued therapy. It is rare for it to cause significant, clinically apparent liver injury. The latency to the onset of liver injury had a median of 155 days, with most cases occurring around 3-4 months after initiation of statin. We describe a patient with statin-induced symptomatic liver injury within one month of statin initiation. Case Description/Methods: A middle-aged woman with past medical history of diabetes mellitus type 2, hypertension, hyperlipidemia, and recent ST-elevation myocardial infarction (STEMI) presented with nausea, vomiting, pruritus, painless jaundice and loss of appetite for over one week. One month prior to her onset of symptoms, she was started on atorvastatin after her STEMI. Her baseline liver biochemistries were normal. Her initial labs on presentation were alkaline phosphatase 2,170, AST 456, ALT 502 and direct bilirubin 10.7, showing a predominantly cholestatic pattern but also with some hepatocellular injury. Atorvastatin was stopped on admission. CT imaging and ultrasound showed liver steatosis and cholelithiasis. No biliary dilatation was seen on MRCP. Other workup was negative, including viral markers and autoimmune studies. Liver biopsy showed sinusoidal dilation/congestion and lymphocytic predominant portal inflammation with eosinophils and plasma cells suggestive of drug-induced liver injury (DILI). She was started on N-acetylcysteine and ursodiol. Her hepatic function initially continued to worsen as noted by high total bilirubin and rising INR, with mildly worsening mental status. She also had acute kidney injury requiring initiation of hemodialysis. Decision was made for expedited liver transplant evaluation. While waiting for the evaluation, she showed gradual improvement in her liver biochemistries and symptoms. Discussion: This case describes a patient who developed statin-induced liver injury within one month of atorvastatin initiation. Although statins can develop mild liver-enzyme elevations, it is rare for it to cause such clinically apparent DILI. Given the widespread use of statins, this case highlights the importance for physicians to closely monitor liver enzymes in patients after initiation of statins.

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