PMC5299161_01
Linear graphs representing the trend of transaminases, INR, and direct bilirubin throughout patient's hospital course and outpatient follow-up.
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fig1
By day two, his transaminases and coagulopathy worsened, with AST 20,176 IU/L, ALT 5,076 IU/L, and INR 3.1 (Figures 1(a), 1(b), and 1(c)).
On Hematoxylin and Eosin stain (100x and 400x), there is centrilobular and bridging necrosis accompanied by portal and lobular inflammation including eosinophils and plasma cells. There is evidence of cholestasis and bile duct injury is noted in some portal tracts. Hepatocellular injury, that is, hepatocyte ballooning degeneration, is also present. Fibrosis is absent on Trichrome staining. There is no evidence of steatosis, glycogenic nuclei, Mallory's hyaline, or copper deposition. Overall, these findings favor a diagnosis of drug-induced liver injury.
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fig2
HHV-6, and HIV), autoimmune workup (ANA, ASMA, AMA, A1AT, IgG, and LTK Ab), metabolic testing (ceruloplasmin, 24-hour urine copper, ophthalmologic examination for Keyser-Fleischer rings, MRI brain to evaluate for lenticular degeneration, and iron studies), urine toxicology, and SPEP/UPEP, was all normal and did not reveal an alternative etiology of the patient's acute liver injury. Abdominal ultrasound demonstrated a 17.4 cm liver with smooth contour and normal echogenicity with patent hepatic and portal vasculature. He underwent a transjugular biopsy which revealed centrilobular and bridging necrosis accompanied by portal and lobular inflammation, favoring drug-induced liver injury (Figures 2(a) and 2(b)).