A 57-year-old female with no previous history of liver disease presented with abdominal pain and vomiting for one day. The abdominal pain was described as 7/10 in severity, nonradiating, and diffuse, but most intense in the right upper quadrant. She denied previously experiencing any similar pain. She denied fever or chills but reported 3 episodes of nonbloody, nonbilious emesis after the pain started. There was a history of heart failure with preserved ejection fraction. She had been taking vitamins A and D and an herbal supplement for weight loss but she denied the use of any prescription weight loss medications. She denied using alcohol, acetaminophen, or any illicit drugs. Her vital signs were normal. Physical examination was significant for diffuse abdominal tenderness without any rigidity or guarding. There was no hepatosplenomegaly or scleral icterus. Laboratory evaluation revealed an alanine aminotransferase (ALT) of 738 U/L [normal: 7-55 U/L], aspartate aminotransferase (AST) of 856 U/L [normal: 8-48 U/L], and an alkaline phosphatase of 80 U/L [normal: 45-115 U/L]. Her total bilirubin was 2.4 mg/dL [normal: 0.1-1.2 mg/dL] and direct bilirubin was 1.4 mg/dL [normal: 0-0.4 mg/dL]. International normalized ratio (INR) was 1.19 [normal: 0.8-1.1] and prothrombin time (PT) was 12.7 seconds [normal 11-13.5 seconds]. Testing for hepatitis A, hepatitis B, hepatitis C, hepatitis E, Herpes-Simplex virus, Ebstein-Barr virus, Parvovirus, and Cytomegalovirus was negative. She had normal vitamins A and D levels ruling out hypervitaminosis as the cause of hepatitis. She tested negative for alcohol and acetaminophen. Anti-smooth muscle antibody, anti-mitochondrial antibody, antinuclear antibody, and anti-liver kidney microsomal antibody were negative. An iron profile was normal. Abdominal ultrasound showed a normal liver with normal echotexture and no biliary ductal dilatation. When the herbal supplement was scrutinized, it was found to be 100% pure GC fruit rind extract. She had consumed two capsules daily as recommended for about one month. Each capsule had 1400 mg of GC extract. She was asked to stop taking the supplement. Her liver enzymes decreased significantly with an ALT of 396 μ/L and AST of 138 μ/L within three days with resolution of her abdominal symptoms. Her total and direct bilirubin came down to 0.6 mg/dL and 0.4 mg/dL, respectively. Her INR and PT also normalized. She had a normal ALT of 25 and AST of 12 in the one-month follow-up visit. Six months later, patient was found to have an elevated ALT of 301 and AST of 69. On interrogation, it was found that she had started taking the same supplement again in the desperate need to lose weight. The CIOMS/RUCAM scale, a scoring system () that is used to establish the etiology of liver damage when drug induced liver damage is suspected, gave a score of 11 for our patient ()[, ]. The score classifies the drug as highly probable (score ≥ 9), probable (score 6-8), possible (score 3-5), unlikely (score 1-2), and excluded (score 0) as the cause of liver injury [, ]. This lead us to conclude that the etiology of the patient's hepatitis was GC extract.
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.