Clinical characteristics and outcome of toxicity from Amanita mushroom poisoning

Abstract

ObjectiveTo describe and analyze the clinical characteristics and outcome of amatoxin poisoning cases.MethodsWe performed a retrospective cohort study of amatoxin poisoning cases from Ramathibodi Poison Center Toxic Exposure Surveillance System, from May 2013 to August 2015.ResultsThere were 30 consultations with a total of 55 poisoning cases. Most cases were male and from the north-east region. Hepatitis, acute kidney injury, jaundice, and coagulopathy accounted for 74%, 46.3%, 44.7%, and 52.8% of the cases, respectively. Almost all of the patients were admitted to the hospital, and the median duration of hospital stay was found to be 4 days. Mortality rate was found to be 27.3%. Most patients (73%) received the treatment including multiple-dose activated charcoal (67.5%), intravenous N-acetylcysteine (87.5%), and benzylpenicillin (45%). In 60% of the cases, the treatment was initiated within 24 h after eating mushrooms. Exchange transfusion and liver transplantation were performed in one severe case. However, this patient died eventually. Because intravenous silybinin is not available in Thailand during the study period, 8 patients received oral silymarin instead. All 8 patients had hepatitis and were treated with high dosage of oral silymarin (5 patients with 4.48 g/day, 2 patients with 1.68 g/day, and 1 patient with 1.4 g/day) for a couple of days. One of these patients died as she received treatment very late; she was treated with silymarin at 1.68 g/day dosage. Thus, the fatality in oral silymarin treatment group was 12.5%. We performed the analysis between the dead and survival groups. We found that in hepatitis, initial and maximum serum aspartate transaminase, initial and maximum serum alanine transaminase, and acute kidney injury were significantly different between the two groups.ConclusionAmanita mushroom poisoning caused high fatalities. Serum transaminase and creatinine were the factors associated with death. Treatment with oral high dose silymarin should be investigated further as one of the principal therapies in amatoxin poisoning.

Milk thistle (Silybum marianum): A concise overview on its chemistry, pharmacological, and nutraceutical uses in liver diseases

“…Also, silymarin can prevent the absorption of toxins into the hepatocytes by occupying the binding sites as well as by inhibiting many transport proteins at the cell membrane. The phalloidin‐transporting system, (which is involved into the incorporation of phallotoxin into the hepatocytes) belonging to the hepatocyte‐specific organic anion uptake transporters OATP2, is inhibited in a competitive way by silymarin with no influence on membrane fluidity (Trakulsrichai et al, ).…”

“…However, uncontrolled trials and several case reports describe successful treatment with an intravenous silybin administration, even in the severely poisoned patients (Mengs, Pohl, & Mitchell, ). Empiric experience suggests the administration of 5 mg/kg silybin every 4 hr for 3–4 days after mushroom ingestion in association with N‐acetylcysteine and multiple‐dose activated charcoal (Karvellas et al, ; Trakulsrichai et al, ).…”

<p>Myotoxic Mushroom Poisoning in Thailand: Clinical Characteristics and Outcomes</p>

“…2,3 Most fatalities are due to amatoxin-containing species, which cause hepatotoxicity and fulminant liver failure. 2,3,[5][6][7] Rhabdomyolysis is a syndrome of mushroom poisoning that is described as either rapid or delayed onset myotoxicity. 2,3 Mushroom poisoning with delayed onset myotoxicity reported in literature is associated with ingestion of selected Tricholoma species, including T. equestre, 2,[8][9][10][11][12] and possibly T. terreum.…”

“…8,[10][11][12]17 In some areas of Thailand, foraging for and consuming wild mushrooms are also popular, contributing to the incidence of mushroom poisoning in our country. 7 Besides amatoxin poisoning, myotoxic mushroom poisoning has significant or severe clinical effects. 21 Clinical data for myotoxic mushroom poisoning are limited.…”

Efficacy of oral Cynara scolymus and Silybum marianum on toxicity of imidocarb dipropionate in horses

“…19 Furthermore, silymarin has been shown to have regulatory actions on the permeability of the mitochondrial membrane and to increase cell membrane stability during xenobiotic injuries. 23 Silymarin also prevents the absorption of toxins by hepatocytes, 24 suggesting potential efficacy in the treatment of liver injuries induced by drugs or toxic substances. Schrieber et al 25 showed that the availability of silymarin and, consequently, its efficacy, varied with the type of liver disease.…”