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 ().
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.