A 36-year-old female with no significant medical history presented with a 3-day history of low-grade fever, nausea, vomiting, and abdominal pain. She reported that she had been following a 500 Kcal diet and was taking GC for four weeks to lose weight. She also complained of fatigue, anorexia, and jaundice. The patient denied any history of recent blood transfusion, illicit drug use, or family history of liver disease. She denied alcohol consumption and was in a monogamous heterosexual relationship.\nOn physical examination, she had scleral icterus, cutaneous jaundice, and tender hepatomegaly measuring 2 cm below the costal margin. Abnormal laboratory results included white blood cell count of 2.73 × 103 cells/μL (4–11) and platelet count of 78 × 103 cells/μL (150–400), aspartate aminotransferase (AST) of 5340 U/L (15–41), alanine aminotransferase (ALT) of 5615 U/L (7–52), alkaline phosphatase of 104 U/L (32–91), total bilirubin of 7.4 mg/dl (0.3–1.0), and direct bilirubin of 4.9 mg/dl (0.0–0.4). Serologies for hepatitis A, hepatitis B, hepatitis C, autoimmune markers (anti-nuclear antibody, anti-smooth muscle antibodies, anti-mitochondrial antibody, and anti-liver kidney microsomal 1 antibody), human immunodeficiency virus, rapid plasma reagin test, cytomegalovirus, Epstein-Barr virus, Herpes Simplex virus, and Parvovirus were negative. Serum ceruloplasmin, alpha-fetoprotein, and alpha-1 antitrypsin levels were normal. Abdominal Doppler ultrasound showed mild echotexture coarsening in the liver and small ascites.\nConsidering her recent exposure to herbal medications, we suspected drug induced liver injury and used updated RUCAM (Roussel Uclaf Causality Assessment Method) scale to calculate its probability. Patient's RUCAM score came out to be 8 points, which is consistent with probable drug induced liver injury []. GC was discontinued and conservative management was initiated. Significant clinical improvement and the downward trend of liver function tests obviated the need for liver biopsy. The patient was discharged on hospital day 6. At follow-up visit two weeks later, her liver function tests had returned to normal ().
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 ).