A 34-year old Hispanic male presented with nausea, vomiting, abdominal pain, and dark urine. Testing revealed elevated transaminases and bilirubin; however, imaging failed to demonstrate cirrhosis or anatomic abnormality. Hepatitis work-up, including testing for viral hepatitis, hemochromatosis, Wilson’s disease, and autoimmune hepatitis, was unremarkable with exception of an elevated Ferritin level of 7089 mg/dL. Genetic testing for hemochromatosis was negative. Medical history was only positive for occasional social alcohol use, and drug toxicology testing was negative. He denied use of energy drinks, herbs, Chinese teas, or muscle milk. He was advised to discontinue alcohol use, which he did, and his symptoms initially seemed to abate.\nSix weeks later, the patient developed asterixis, jaundice, and confusion. Follow-up imaging was concerning for rapid onset of cirrhosis or infiltrative hepatocellular carcinoma. He was transferred to our center for further evaluation. On admission, transaminases were elevated with aspartate aminotransferase (AST) 624 U/L, alanine aminotransferase (ALT) 520 U/L and total bilirubin of 34.7 mg/dL. International normalized ratio (INR) remained elevated despite multiple infusions of fresh frozen plasma and vitamin K. Factor Vand VII activities were 18% and < 6%, respectively. Magnetic resonance imaging (MRI) with Eovist contrast demonstrated interval development of heterogeneous, enhancing nodularity with portal venous washout, unlikely to be an infiltrative tumor process.\nA full repeat hepatitis work-up was performed (Table ). No definitive cause of acute liver failure could be identified; however, some findings were equivocal. Autoantibody titers demonstrated a positive antinuclear antibody, but no other positive autoantibodies. Evaluation of Wilson’s disease demonstrated normal ceruloplasmin and copper levels; however, 24-h urine copper was elevated. Serum ferritin but not transferrin was elevated.\nLiver biopsy was performed and demonstrated submassive necrosis with collapse of the hepatic architecture involving about 70% of the liver parenchyma. Mild lymphocytic inflammatory infiltration and minimal canalicular cholestasis were seen. No viral inclusions or other infectious agents were identified by histology or immunohistochemistry. No evidence of granuloma, tumor, or features of cirrhosis were demonstrated. Periodic acid-Schiff (PAS) stain with diastase was negative for alpha-1 antitrypsin globules. Iron stain showed only mild iron deposition in Kupffer cells and hepatocytes. Quantitative tissue copper was within normal limits (Table ). Findings were felt to be potentially related to drug-induced liver injury.\nAfter extensive questioning, the patient divulged intake of Garcinia cambogia, purchased through the Internet retailor Swanson Vitamins. He imbibed two 80 mg capsules of “Garcinia Cambogia 5:1 Extract” three times daily before meals for five months preceding initial presentation. Since not advised against intake, he continued the supplement after initial presentation. He denied any other medications or supplements and reported no alcohol intake for two months.\nThe patient’s status declined and his mental status deteriorated. He was listed status 1A for liver transplantation. He received an orthotopic liver transplant from an ABO-identical brain dead donor and has recovered without incident. Histopathologic examination of the explanted liver demonstrated near total hepatic necrosis with massive hepatocellular dropout and mixed inflammatory cell infiltrates, consistent with severe drug-induced liver injury (Figure ).
A 22-year-old obese female presented to the emergency department with complaints of chest pain, progressive fatigue, palpitations and shortness of breath for two days. She also noticed tremors in her hands. She denied any abdominal pain, nausea, vomiting, fever, chills or rash. She reported taking a herbal supplement for weight loss, named Proclinical Hydroxycut, two capsules daily for about three months. She denied alcohol use, recent travel, other medications/supplements, family history of autoimmune diseases.\nOn admission, vitals were significant for tachycardia with heart rate 113 beats per minute and oxygen saturation was 84% on room air. Physical examination was remarkable for obesity with body mass index (BMI) 41, mild asterixis bilaterally. No encephalopathy, scleral icterus or hepatosplenomegaly was found. Laboratory analysis showed leukocytosis with white blood cell count of 24 x 103/ul (4.4-10.5 103/ul), severe transaminitis with alanine aminotransferase (ALT) 2399 U/L (4-51 U/L), aspartate aminotransferase (AST) 4040 U/L (5-46 U/L),alkaline phosphatase level 72 U/L (40-129 U/L), total bilirubin 0.6 mg/dl (0.1-1.5 mg/dl), International Normalized Ratio (INR) 1.4 (0.8-1.2).\nInvestigations for other etiologies of acute liver injury including hepatitis panel, Tylenol level, antinuclear antibody, anti-smooth muscle antibody, anti-mitochondrial antibody, ceruloplasmin level, ferritin level, and serologies for Ebstein-Bar virus (EBV), herpes simplex virus (HSV) and cytomegalovirus (CMV) were unremarkable. Abdomen Ultrasound showed hepatomegaly and doppler studies of the liver were unremarkable (Figure ). Computed tomography (CT) scan of the chest showed developmental abnormalities like scoliosis and lung hypoplasia (Figure ).\nShe was diagnosed with acute drug-induced liver injury likely due to Hydroxycut and treated with N-acetylcysteine. Transaminases trended down during the course of hospitalization after Hydroxycut was stopped and levels were ALT 189 and AST 61 on day 8 (Figure ). She was discharged in stable condition to follow up outpatient with hepatology.