Treating Amanita phalloides poisoning: is silibinin superior to chicken dung?

January 24, 2013, 11:17 pm

Milk thistle

★★½☆☆

Amanita phalloides poisoning and treatment with silibinin in the Australian Capital Territory and New South Wales. Roberts DM et al. Med J Aust 3013 Jan 21;198:43-47

Abstract

In one of his published works, the second-century Roman physician Galen related an anecdotal method of treating mushroom poisoning:

I have heard of a physician of Mysia who administered Fowl’s dung to persons suffering form fungus poisoning, and I myself have experimented with the remedy. I have used finally powdered dung mixed with water or mixed with honey and vinegar The patients immediately on drinking the mixture vomited and recovered. One must observe that the dung of a fowl at liberty is more efficacious than one in confinement.

             

Unfortunately, in the two millennia since Galen advocated the therapeutic benefits of ingesting chicken dung (and free-range chicken dung at that!) we really haven’t discovered any specific antidotes with proven efficacy. Not that possible candidates have not been put forward.  High-dose penicillin-G, thioctic acid, dexamethasone, cimetidine, N-acetylcysteine (NAC), silymarin, and silibinin have all been tried; none has been proven to improve clinical outcomes.

Silibinin and silymarin are extracts of the milk thistle plant (Silybum marianum). It is thought that silibinin may inhibit entry of amatoxin into hepatocytes through cell membrane receptors.

This observational retrospective case series looked at patients admitted to certain Australian hospitals for suspected Amanita phalloides poisoning  over a 12-year period. Of the 12 patients identified,  10 received silibinin. Four died of fulminant hepatic failure and shock. Additional treatments included IV fluids, multidose activated charcoal, penicillin, cimetidine, and silymarin.

Unfortunately, there is nothing of value one can deduce from this type of observational study, whick looked at only a small number of patients managed with non-standardized treatment. Certainly, silibinin didn’t prevent the sickest patients from dying: all patient who died — but none of the survivors — had lactate levels > 10 mmol/L. Despite this, the authors recommend “treatment with supportive care, multiple doses of activated charcoal, intravenous silibinin, and acetylcysteine, as well as consideration of liver transplantation.” All of these suggestions seem reasonable except for the IV silibinin, which is not stocked by many hospitals and is often difficult to obtain. It seems to me there are more important things to do when taking care of these sometimes very sick patients.

Surprise quiz! Here are some questions about A. phalloides toxicity touch on in the article. (Click on the question to reveal the answer.)

0-6 hours: asymptomatic

6-24 hours: gastroenteritis, dehydration.

1-7 days: resolving GI symptoms, but progressive hepatotoxicity, coagulopathy, renal failure.

> 7 days: resolution if patient survives.

Amatoxin undergoes enterohepatic recirculation.

The Meixner test detects the present of amatoxin. Hydrochloric acid is added to a sample of juice squeezed from the mushroom and absorbed on a newspaper. A blue color suggests the presence of amatoxin, but is not specific.

Related post:

Silibinin or Silly Putty for Mushroom Poisoning?

 

 

[Photograph of milk thistle from wikipedia.org]

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