Biphasic amatoxin poisoning — 6–24h latent, GI phase, deceptive false recovery, hepatorenal failure day 3–5. What ER teams do, and when to call poison control.
Amanitin (alpha-amanitin, beta-amanitin, gamma-amanitin) is the group of cyclic octapeptide toxins produced by Amanita phalloides ("death cap"), Amanita virosa ("destroying angel"), Galerina marginata ("deadly Galerina"), and several Lepiota species. These toxins cause acute liver failure that begins silently and can kill within a week without treatment. Alpha- amanitin binds RNA polymerase II, halting messenger-RNA production. Cells with high protein turnover — liver hepatocytes, then kidney tubular cells — die over 48 to 96 hours.
No symptoms. Patients feel completely normal. Amanitin has been absorbed and is already inside hepatocytes binding RNA polymerase II. This is the window where treatment is easiest and most effective — and the window when most people incorrectly assume they are safe.
Sudden violent vomiting. Profuse, cholera-like watery diarrhoea. Abdominal cramps. Rapid dehydration and electrolyte loss. The American College of Emergency Physicians specifically flags delayed-onset (past 6 hours) GI symptoms after a mushroom meal as one of the presentations that should raise amatoxin suspicion.
GI symptoms subside. Patients feel much better and frequently request discharge. Liver enzymes (AST, ALT), bilirubin, and INR are climbing during this window; hepatocyte death continues silently. Premature discharge in this window is a well-documented cause of preventable death.
Jaundice, coagulopathy, hypoglycaemia, encephalopathy, acute liver failure. Renal failure follows in many patients. Survival depends on how early supportive care started and how quickly the patient reaches a hospital with a liver-transplant service.
Alpha-amanitin is heat-stable, acid-stable, freeze-stable, and dry- stable. Cooking does not destroy it. Drying does not destroy it. Freezing does not destroy it. Tea preparation does not destroy it. There is no home preparation that reduces the risk. It also does not irritate the mouth or stomach on contact — patients absorb the toxin without any warning taste or nausea. By the time symptoms appear, hours of enterohepatic recirculation have re-delivered the toxin to the liver repeatedly.
There is no single approved antidote for amanitin poisoning. Standard care per clinical toxicology references and ACEP guidance combines several interventions:
| Intervention | Purpose | When used |
|---|---|---|
| Aggressive IV fluid resuscitation | Correct GI-loss dehydration and support renal perfusion | From ED arrival |
| Multi-dose activated charcoal | Interrupt enterohepatic recirculation of amanitin | If patient presents early or GI still active |
| Silibinin (Legalon) | Blocks hepatocyte uptake of amanitin (OATP1B3 inhibition) | Available through expanded-access programme in US; standard care in EU |
| N-acetylcysteine | Antioxidant and hepatic glutathione support | Standard adjunct |
| Serial LFTs, INR, glucose | Track hepatocyte death and coagulopathy | Every 6–12 hours |
| Transfer to transplant centre | Access to King's College / Clichy criteria evaluation | If AST/ALT and INR trend worsening |
Silibinin (a purified milk thistle flavonolignan) is standard of care in much of the European Union and is accessible in the US through an expanded-access programme run by Mithridion / Legalon SIL via participating poison centres. If your hospital does not have silibinin on formulary, the poison centre call can find the nearest supply.
Call poison control before symptoms start. In the US that is 1-800-222-1222, free, 24 hours a day. The reason is time: interventions are dramatically more effective during the latent phase than after liver damage is established. A poison-centre toxicologist can also identify the closest silibinin supply and the closest transplant centre if the case worsens.
Outcomes vary widely with the amount ingested, patient age, and how quickly treatment starts. Modern series in centres with silibinin access report survival above 80% when treatment begins in the latent or early GI phase; historical series before silibinin and standardised supportive care reported mortality of 20–30%. Paediatric outcomes are generally worse because dose per kilogram is higher. See summaries in Ye and Liu (2018) and the NAMA Toxicology Committee reports.
Amanitin is a family of cyclic octapeptide toxins (alpha-, beta-, and gamma-amanitin) produced by several genera of mushrooms — Amanita, Galerina, and some Lepiota. It binds RNA polymerase II inside cells and stops protein synthesis. Liver and kidney cells are affected first.
Usually 6 to 24 hours. That long, silent delay is the single most dangerous feature of amatoxin poisoning. Symptoms starting within the first two hours after a mushroom meal usually indicate a different toxin (gastroenteric syndromes from other genera).
No single approved antidote. Silibinin (Legalon) blocks hepatocyte uptake of amanitin and is standard of care in the EU; it is accessible in the US through an expanded-access programme. N-acetylcysteine, aggressive IV fluids, and early transplant referral are combined with silibinin.
Yes, especially with early treatment. Modern series with silibinin access report survival above 80% when care starts during the latent or early GI phase. Delayed presentation, high dose, or paediatric cases have worse outcomes. Liver transplant is the last-resort option for fulminant hepatic failure.
Around day 2 after ingestion, the GI phase resolves and patients feel dramatically better. Liver enzymes and INR are climbing during this window while hepatocytes continue to die silently. Patients often try to leave hospital during false recovery. Discharging them here is a documented cause of preventable death.
No. Amanitin is heat-stable, acid-stable, freeze-stable, and dry- stable. Cooking, drying, tea preparation, and freezing do not reduce toxicity. This is the specific molecular property that makes amatoxin mushrooms so dangerous compared to other risky foods.
No. They are unrelated. Psilocybin is not systemically toxic in the way amanitin is; the risks are psychological and cardiovascular, not hepatic failure. Amanitin poisoning shows up in people who thought they had picked psilocybin mushrooms and picked Galerina marginata instead. That is why the two topics share this cluster of pages.
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