A 27-year-old man with no significant past medical history presented as a referral from a community hospital for evaluation of hepatitis, initially diagnosed as choledocholithiasis. The patient complained of fever, chills, and abdominal pain (achy in the Right Upper Quadrant and epigastrium) for the past 2 weeks, nausea, and vomiting of clear liquids without blood for a 1 week, and jaundice for 2 days. Records from referring facility indicated that patient had MRCP-Magnetic Resonant Cholangio Pancreatography that demonstrated cholelithiasis, but it did not show any signs of cholecystitis. An abdominal ultrasound revealed sludge and gallstones in the gallbladder.\nFurther questioning revealed that patient had been studying to be a physical trainer at a local college. He exercised vigorously at least 3 times/week. Patient stated that he was “prescribed” a set of supplements (Hydroxycut, Black powder, mitotropin, xenadrine, arson, and L-glutamine powder 23) by his local nutrition center.\nAfter admission in the hospital, hepatology consult was called. When patient was admitted, liver enzymes panel showed: AST-Aspartate Aminotransferase: 3800 U/L, ALT-Alanine aminotransferase: 5100 U/L, total bilirubin: 14.7 mg/dl, direct bilirubin: 10.0 mg/dl and alkaline phosphatase: 99 mg/dl, all correlated with the degree of jaundice seen. Additional tests included a urine toxicology screen, immunological studies for liver (anti-nuclear antibodies, anti-smooth muscle antibodies, and anti A liver/kidney microsomal antibodies), serum acetaminophen level, serum ceruloplasmin level, and genetic tests for hemochromatosis; all of them were negative. Liver biopsy showed signs of acute liver failure.\nHematoxylin and eosin stain of the liver biopsy specimen is shown in Figures and . shows extensive patchy areas of necrosis as in acute fulminant hepatitis with sparing of biliary tract. shows lymphocytic infiltration of the portal tracts and lobular parenchyma.\nPatient was asymptomatic during the hospital stay and was planned to discharge with trending down of liver enzymes by discontinuation of Hydroxycut and conservative management. The patient was advised to follow-up with Hepatology. On follow-up visit after 2 weeks of discharge, Labs: AST: 669 U/L, ALT: 1965 U/L, Total Bilirubin: 4.5 mg/dl, Alkaline phosphatase: 128 mg/dl, PT: 1.1.
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 ).