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 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.