While detection of amanitins is important in the diagnosis, there is no correlation between plasma concentration and clinical outcome.
More definitive detection of amanitins has been demonstrated with capillary zone electrophoresis, ELISA assays of urine, and LC-MS/MS/MS of serum and liver extracts.
Amanitin poisoning is distinguished bythree clinical stages: an incubation stage, a gastrointestinal stage and a cytotoxic stage.
Administration of cimetidine, a cytochrome P-450 inhibitor which inhibits the uptake of amatoxins by the mixed function oxidase system, and N-acetylcysteine (NAC), a glutathione precursor that binds amatoxin-related free radicals, have also been used in the treatment of amanitin intoxication.
Methods for chromatographic determination of amanitins and related toxins in biological samples.
Silymarine (from the milk thistle Silibum marianum) exerts its protective effect after intravenous administration in various ways: (a) by interrupting the enterohepatic recirculation of amanitin; (b) by inhibiting the binding of toxins to hepatocyte membranes; (c) by competing with amatoxin for transmembrane transport; and (d) by inhibiting the penetration of amanitin into liver cells (1).