A 21-year-old African American female with noted obesity (basic metabolic index 40.34 kg/m2), without significant past medical history, presented with abdominal pain for 1 wk.\nHer abdominal pain was described as 7 out of 10 on a pain scale, diffuse, and non-radiating. It was associated with nausea, multiple episodes of non-biliary and non-bloody vomiting, anorexia, and myalgias. She denied any jaundice, pruritis, change in bowel habits, urinary symptoms, or extremity swelling. There was no history of fever, sick contacts, or recent blood transfusions.\nThere was no significant past medical illness.\nShe denied smoking tobacco, drinking alcohol, usage of illicit drugs, hormonal contraceptives, or energy drinks. She mentioned that she was taking a HS, GC (1400 mg daily), for weight loss since 4 wks. Family history was unremarkable.\nVital signs were notable for tachycardia (133 bpm). On examination, she had epigastric and right upper quadrant tenderness, without jaundice or hepatosplenomegaly.\nLaboratory workup (Table ) revealed elevated alanine aminotransferase (ALT) 981 U/L, aspartate aminotransferase (AST) 1062 U/L, alkaline phosphate 248 U/L, international normalized ratio (INR) 1.6, prothrombin time 19 s, and ammonia level 44 μmol/L. Acetaminophen and alcohol levels were negative, as was her urine toxicology. Testing for hepatitis A, hepatitis B, hepatitis C, human immunodeficiency virus, herpes simplex virus, cytomegalovirus, Epstein Barr virus, parvovirus, and rapid plasma regain were negative. Autoimmune work-up including antinuclear antibody, antimitochondrial antibody, and anti-smooth muscle antibody were also negative. Serologies for alpha-1 antitrypsin, ceruloplasmin, iron studies, alpha fetoprotein, and carcinoembryonic antigen were unremarkable.\nAbdominal ultrasound showed hepatosplenomegaly with heterogenous increased echogenicity compatible with fatty liver. Abdominal computer tomography (CT) scan showed hepatosplenomegaly with heterogeneous-appearing liver.
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 ).