Abstract
More than 90% of all fatal mushroom poisonings worldwide are due to amatoxin containing species that grow abundantly in Europe, South Asia, and the Indian subcontinent. Many cases have also been reported in North America. Initial symptoms of abdominal cramps, vomiting, and a severe cholera-like diarrhea generally do not manifest until at least six to eight hours following ingestion and can be followed by renal and hepatic failure. Outcomes range from complete recovery to fulminant organ failure and death which can sometimes be averted by liver transplant. There are no controlled clinical studies available due to ethical reasons, but uncontrolled trials and case reports describe successful treatment with intravenous silibinin (Legalon® SIL). In nearly 1,500 documented cases, the overall mortality in patients treated with Legalon® SIL is less than 10% in comparison to more than 20% when using penicillin or a combination of silibinin and penicillin. Silibinin, a proven antioxidative and anti-inflammatory acting flavonolignan isolated from milk thistle extracts, has been shown to interact with specific hepatic transport proteins blocking cellular amatoxin re-uptake and thus interrupting enterohepatic circulation of the toxin. The addition of intravenous silibinin to aggressive intravenous fluid management serves to arrest and allow reversal of the manifestation of fulminant hepatic failure, even in severely poisoned patients. These findings together with the available clinical experience justify the use of silibinin as Legalon® SIL in Amanita poisoning cases.
Highlights
Human poisoning with cytotoxic mushrooms (Amanita phalloides and related species) is associated with severe morbidity and a high mortality rate due to rapidly progressive fulminant hepatic failure.While fatal mushroom poisoning has long been recognized as a major health problem in Europe, the gathering and consumption of wild mushrooms is popular in some immigrant populations as well as mushroom enthusiasts in the US leading to an increasing health hazard [1, 2]
Human intoxication with Amanita phalloides and related species is associated with severe morbidity and a high mortality rate due to progressive fulminant hepatic failure
Given the similarity to human intoxication pathology, the reduction of liver cell damage measured by laboratory parameters, histology and mortality rates after intravenous application of silibinin in a pharmacological dog model is noteworthy
Summary
Human poisoning with cytotoxic mushrooms (Amanita phalloides and related species) is associated with severe morbidity and a high mortality rate due to rapidly progressive fulminant hepatic failure. Amanita mushrooms have been ingested in suicide attempts [3]. Epidemiological data on mushroom poisoning, poisoning with amatoxin-containing mushrooms, are rare. In the case of intoxication with Amanita species - the most relevant being Amanita phalloides - the summary of typical clinical symptoms is called phalloides syndrome. (Table 1) lists the Amanita species responsible for the great majority of all fatal mushroom poisonings found throughout Europe and increasingly in North America [5, 2]. Ingestions and deaths from other amatoxin containing genera like Lepiota and Galerina have been reported [7, 8]. Prior to the 1980s the mortality rate following amatoxin ingestion was reported to be higher than 50%. Over the past 25 years the mortality rate has been reduced to 10-20% primarily due to improved supportive and intensive care [2]
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