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 ).
An 82-year-old man with a past medical history significant for obesity, AP secondary to cholelithiasis, prior cholecystectomy, hypertension, hyperlipidemia, diabetes mellitus, pulmonary embolism, and nonischemic cardiomyopathy presented to the emergency department with concerns of abdominal discomfort for two days. The patient reported discomfort in the epigastric region, which was non-radiating. He reported nausea but no vomiting. He reported at least two bouts of AP in the past. The patient denied any fevers, chills, lightheadedness, headaches, chest pain, shortness of breath, hematochezia, numbness, or melena. His medications included aspirin, apixaban, atorvastatin, metformin, metoprolol, spironolactone, and ramipril.\nThe patient reported taking GC as an appetite suppressant. On physical exam, tenderness was noted in the epigastric area, and bowel sounds were positive. His serum lipase was elevated to >600 U/L (reference range, 16 to 63 U/L), white blood cell count was 11.7 K/µL (reference range, 4.5 to 11 K/µL), hemoglobin was 13.4 g/dL (reference range, 13.5 to 17.5 g/dL), bilirubin was 0.5 mg/dL (reference range,0.1 mg/dl to 1.2 mg/dl), alkaline phosphatase was 66 IU/L (reference range 44 to 147 IU/L), alanine aminotransferase was 12 U/L (reference range, 10 U/L to 40 U/L), aspartate aminotransferase was 17 U/L (reference range, 10 to 40 U/L), and lactic acid was 0.9 mmol/L (reference range, 0.5 to 2.0 mmol/L). A computed tomography scan of the abdomen revealed fat stranding around his pancreas, which was concerning for AP (Figure ).\nThe patient denied any use of alcohol. Triglycerides levels were 146 mg/dL (reference range, <200 mg/dL). He was hospitalized and treated with adequate intravenous hydration, nothing by mouth, with remarkable improvement in his symptoms within 24 hours of presentation. He tolerated regular oral diet on discharge from the hospital. Due to his relatively recent consumption of GC and no recent changes in any other medications, a likely etiology of AP was thought to be secondary to the use of this herbal product. His care team recommended he avoid the use of GC in the future.