A liver transplant candidate (fulminant hepatic failure from amanita phalloides poisoning) as a multiorgan donor

LIVER transplantation is now a well-established treatment in patients with fulminant hepatic failure (FHF) due to poisoning by mushrooms containing amatoxins.’ Amatoxins are a group of chemically defined octapeptides with a molecular weight of 900 Dalton? and are present in different species of wild mushrooms (Amanita phalloides, Amanita virosa, Amanita vema, Lepiota sp., or Galerina matginata). In the case of human poisoning with such mushrooms amatoxins are considered the sole cause of liver damage. Amatoxins produce necrosis of eukaryotic cells by binding to nuclear RNA polymerase B and inhibiting enzymatic activity.” Although amatoxins are equally toxic to all cells, in human poisoning they exhibit an apparent specific toxicity to intestinal epithelium, hepatocytes, and possibly to the kidneys.” The mechanism of toxin uptake is not clear but the mechanism responsible for the physiologic bile salt transport seems to be involved.4 Amatoxins have been evaluated by radioimmunoassay in the serum of poisoned patients up to 36 hours from ingestion” with values of few ng/mL. Because the toxins are eliminated through bile and urine, higher concentrations than in serum have been found in gastric juice6 and urine.5