The consumption of wild mushrooms of the amanita genus produces liver toxicity and fulminating liver failure in different geographical areas, including Chile, where, as well as the Amanita phalloids, intoxication by the Amanita gemmata variety is well documented (1,2). Cases of poisoning have risen, possibly due to the growing use of mushrooms for hallucinogenic purposes.
Aspect of the mushroom Amanita phalloides
The Amanita phalloid is the variety which most often causes poisoning (90%). The mushroom grows in humid and shady places. Its color varies, from grayish brown to yellow or greenish, with white laminas under the cap. It is important to emphasize that it can be very difficult to distinguish between these and other edible mushrooms.
Pathogenesis
The amanita has at least two potent types of toxins: amatoxins and phallotoxins, which are bicyclic peptides. Amatoxins cause hepatocellular damage thanks to their capacity to inhibit the RNA enzyme topoisomerase II, blocking the transcription of genes in the nucleus of the hepatocyte. The alpha-amanita is extremely toxic: 5 mg are capable of producing the death of an adult. An average pileo (‘cap’) contains 30 to 90 mg of this substance. The alpha-amanita can be detected by radioimmunoassay in blood or urine, although this is not performed as a routine test. The toxins are not inactivated with heating or cooking.
Clinical presentation
Typical clinical presentation is described as a three stage process from the moment of ingestion (3):
- First stage (6 to 4 h): The predominating symptoms are abdominal pain, nausea, vomiting, diarrhea, fever, dehydration, hypotension and hydroelectrolytic disturbance.
- Second stage (24 to 48 h): The initial symptoms improve, although the hepatic and renal disturbance may continue to progress.
- Third stage (3 to 5 days): Jaundice, encephalopathy and liver failure. Mortality associated with ingestion is from 20 to 30%.
Treatment
There is no specific antidote which is demonstrably effective. Silymarin, high dose penicillin and N-acetylcysteine (NAC) have been used, but the usefulness of these approaches is debated. Hemodialysis and hemoperfusion can eradicate the toxin if it is started early. Similarly it is possible that systems of hepatic dialysis of albumin (MARS) may be effective. The only useful treatment demonstrated in circumstances of acute hepatic insufficiency and if the normal criteria are fulfilled is liver transplant (4).
References
- Zaror M, Sanhueza E, Reynolds E, Hepp J, Ríos H, Suárez L. Falla hepática fulminante por Amanita phalloides. Gastr Latinoam 1999;10:330.
- Sierralta A, Jeria ME, Figueroa G, Pinto J, Araya JC, San Juan J, Grinbergs J, Valenzuela E. Intoxicación por callampas venenosas en la IX Región. Rol de Amanita gemmata. Rev Med Chil 1994;122:795-802.
- Koppel C. Clinical symptomatology and management of mushroom poisoning. Toxicon 1993;31:1513-40.
- Klein AS, Hart J, Brems JJ, Goldstein L, Lewin K, Busuttil RW. Amanita poisoning: treatment and the role of liver transplantation. Am J Med 1989;86:187-93.
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