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.
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.