A 22-year-old obese female presented to the emergency department with complaints of chest pain, progressive fatigue, palpitations and shortness of breath for two days. She also noticed tremors in her hands. She denied any abdominal pain, nausea, vomiting, fever, chills or rash. She reported taking a herbal supplement for weight loss, named Proclinical Hydroxycut, two capsules daily for about three months. She denied alcohol use, recent travel, other medications/supplements, family history of autoimmune diseases.\nOn admission, vitals were significant for tachycardia with heart rate 113 beats per minute and oxygen saturation was 84% on room air. Physical examination was remarkable for obesity with body mass index (BMI) 41, mild asterixis bilaterally. No encephalopathy, scleral icterus or hepatosplenomegaly was found. Laboratory analysis showed leukocytosis with white blood cell count of 24 x 103/ul (4.4-10.5 103/ul), severe transaminitis with alanine aminotransferase (ALT) 2399 U/L (4-51 U/L), aspartate aminotransferase (AST) 4040 U/L (5-46 U/L),alkaline phosphatase level 72 U/L (40-129 U/L), total bilirubin 0.6 mg/dl (0.1-1.5 mg/dl), International Normalized Ratio (INR) 1.4 (0.8-1.2).\nInvestigations for other etiologies of acute liver injury including hepatitis panel, Tylenol level, antinuclear antibody, anti-smooth muscle antibody, anti-mitochondrial antibody, ceruloplasmin level, ferritin level, and serologies for Ebstein-Bar virus (EBV), herpes simplex virus (HSV) and cytomegalovirus (CMV) were unremarkable. Abdomen Ultrasound showed hepatomegaly and doppler studies of the liver were unremarkable (Figure ). Computed tomography (CT) scan of the chest showed developmental abnormalities like scoliosis and lung hypoplasia (Figure ).\nShe was diagnosed with acute drug-induced liver injury likely due to Hydroxycut and treated with N-acetylcysteine. Transaminases trended down during the course of hospitalization after Hydroxycut was stopped and levels were ALT 189 and AST 61 on day 8 (Figure ). She was discharged in stable condition to follow up outpatient with hepatology.
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.