[Review of present knowledge on the pathogenesis and pathophysiology of Amanita phalloides poisoning]

The mushroom poisoning of phalloid type is caused by amatoxins, mainly by alpha-amanitine. It is a cytotoxin which acts through an indirect mechanism. It binds irreversibly the nucleolar enzyme, RNA-polymerase II in cells with intensive proteosynthesis (enterocytes in the digestive tract, hepatocytes in the liver and epithelial cells of proximal renal tubules). A tight binding of the toxin with the enzyme blocks the transcription from DNA to m-RNA and thus makes the proteosynthesis impossible. This results in the cell necrosis. Pathophysiology of the phalloid type poisoning is rather complicated, as the disorders of primarily affected organs (gastrointestinal tract, liver and kidney) produce a derangement of other remote organs and systems. After a relatively long period of latency (average 8-10 hours) the symptoms of the initial phase of the symptomatologic course of intoxication--excessive vomiting and diarrhea (during one or two days)--are observed, leading to dehydration which culminates in the hypovolemic shock. A short subsequent phase of an apparent improvement (in the 3rd day) is followed, beginning with the fourth day, by an acute failure of the liver and kidney. The cause of the failure of both the organs is the same--the toxic noxa. Therefore it is not possible to classify the coexistence of acute hepatal and renal failure as a so-called hepatorenal syndrome. The true hepatorenal syndrome is namely a potentially reversible prerenal failure accompanying a variety of serious liver diseases, namely in their terminal phase. The phalloid nephropathy, however, has two constituents.(ABSTRACT TRUNCATED AT 250 WORDS)