Copper studies of liver biopsy were not performed. Birinapant (TL32711) == Physique 1. [2]. We describe a case of severe hepatotoxicity with jaundice and moderate synthetic dysfunction in a patient taking multiple dietary supplements. == 2. Case == A previously healthy 45-year-old white male complained of dull aching RUQ pain associated with nausea two weeks prior to his initial demonstration to primary care. The pain was constant, nonradiating, and most intense two hours after meals. The pain was followed by icterus, jaundice, and generalized some weakness, which gradually worsened on the week. He had secondary anorexia on the symptomatic period and experienced lost 20 lbs over the previous two months. He denied pruritus, easy bleeding/bruising, melena, abdominal distention, mental status changes, increased somnolence, diarrhea, or fever. He initially reported taking only a few daily health supplements over the previous 12 months for the promotion of general health. However, on further questioning, he admitted using nine different products many of which had been started one-to-four months prior to his symptom onset (Table 1). He had stopped all health supplements intake after the development of his symptoms. == Table 1. == Reported health supplements in this case. Additional risk factors for secondary causes of liver disease were bad to include a history of viral hepatitis, blood product transfusion, Birinapant (TL32711) intravenous drug abuse, multiple lovemaking partners, and prescription medications. He consumed two-to-three combined drinks on social occasions and was not a habitual alcohol consumer. He denied acetaminophen use or the ingestion of crazy mushrooms. He recently vacationed with his wife in Puerto Rico three months prior to demonstration but denied any additional foreign travel. He had no Birinapant (TL32711) family history of liver disease and denied any ill contacts. His physical exam was only notable for jaundice, scleral icterus, and moderate RUQ abdominal tenderness on deep palpation. Significant demonstration labs are as follows: ALT 6409 U/l, AST 3505 U/l, alkaline phosphatase 269 U/L, total bilirubin 31 mg/uL, conjugated bilirubin 18 mg/dL, prothrombin time 12.6 sec, and INR 1.2. Iron studies were ferritin 2641 ng/mL, fasting iron 235 ug/dL, TIBC 290 ug/dL, and % transferrin sat 81%. CBC was normal without eosinophilia. Serum acetaminophen level Birinapant (TL32711) was immeasurable as the severe hyperbilirubinemia interfered with the assay. The patient did not possess any baseline liver enzymes for assessment. RUQ ultrasound and CT belly revealed moderate diffuse thickening of the gallbladder without cholelithiasis or intra/extrahepatic ductal dilatation. The pancreas, liver, portal veins, and spleen were otherwise normal. The workup for other causes of liver disease includes IgM anti-HAV, IgM anti-HBc, HbsAg, anti-HCV, ceruloplasmin, mitochondrial antibody, ANA, SPEP, and anti-LKM which were negative/normal except for the presence of one heterozygous copy of the H63D mutation in the HFE gene MEN2A and a highly positive smooth muscle mass antibody of 32 (>30 highly positive). Liver histopathology revealed moderate periportal and intraparenchymal chronic swelling, including plasma cells, with focal areas of acute swelling and patchy hepatocyte necrosis with moderately increased iron storage (Iron liver dry weight 321 ug/g (4002200) hepatic iron index 0.1 umoL/g/yr (<1.0)) (Physique 1). Copper studies of liver biopsy were not performed. == Physique 1. == (a) Periportal triad swelling (b) cholestasis and hepatocyte necrosis (zone 3) iron liver 321 ug/g dry wt (4002200), hepatic iron index 0.1 umoL/g/yr (<1.0). The liver biopsy was secondarily examined from the Armed Forces Institute of Pathology that reported common zone 3 (centrilobular) confluent necrosis and stromal collapse with patchy portal swelling and substantial bile stasis. Their interpretation of the combined cholestatic and hepatocellular injury pattern was consistent with drug/supplement-related hepatotoxicity. The findings were not consistent with autoimmune hepatitis. At 6 weeks, the patient's symptoms experienced resolved. Replicate liver-associated enzymes experienced.