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 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.