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Elderberry
The second, more important, category of mushrooms, which are responsible for
90% of mushroom-related deaths, are those typically associated with onset of
symptoms that occur more than 6 hours after ingestion. The most important
members of this group are those mushrooms that belong to the Amanita
phalloides species. With these mushrooms, after a latent period of many hours, GI
upset appears. Approximately 24 hours after ingestion, hepatic dysfunction
appears, which may progress to fulminant hepatic failure. Without liver
transplantation, such patients generally die. One other Amanita mushroom, A.
smithiana, causes symptom onset prior to 6 hours, and then patients can develop
renal failure more than 24 hours postingestion. In areas where A. smithiana can
be found (the Pacific Northwest), risk stratification based on delayed onset of
symptoms is not reliable.
Two compounds produce the toxic effects of A. phalloides. Phallotoxin acts
first, causing nausea, vomiting, abdominal pain, and diarrhea. Fever, tachycardia,
and hyperglycemia may also occur during this stage. The other toxin, amatoxin,
causes renal tubular and hepatic necrosis.
Treatment of the gastroenteric phase includes fluid and electrolyte replacement.
If renal failure develops, dialysis may be necessary. Hepatic damage after A.
phalloides ingestion may be attenuated by early use of repetitive activated
charcoal, which appears to interrupt enterohepatic recirculation of amatoxin.
Additional therapies have shown mixed results in the treatment of A. phalloides
poisoning. High-dose penicillin, Polymyxin B, cimetidine, N -acetylcysteine,
thioctic acid, silibinin, prophylactic charcoal hemoperfusion, and other modalities
await further investigation. A regional poison control center may offer guidance
with experimental therapies, but multiple-dose activated charcoal and vigorous
attention to supportive care remain the standard. For patients with poor prognosis,
early referral for liver transplantation may be lifesaving.

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