Herbal products found in nature can serve as great systems of study for drug design. The Amanita muscaria mushroom is native to many parts of the Northern Hemisphere and has a very distinctive appearance with its red cap and white spotted warts. The mushroom comprises several pharmacologically active alkaloids, including muscazone, muscarine, ibotenic acid, and muscimol, the latter two compounds being potent GABA agonists. Muscimol has served as a backbone in the design of GABA agonists devoid of effects on the GABA-metabolizing enzyme, GABA transaminase, and GABA uptake systems. In this sense, several analogs of muscimol have been synthesized and studied including THIP, THPO, iso-THIP, iso-THAZ and 4-PIOL which all interact with the GABA receptors much differently. The growing pharmacological and toxicological interest based on many conflicting opinions on the use of the neuroprotective role of muscimol analogs against some neurodegenerative diseases, its potent role in the treatment of cerebral ischemia and other socially significant health conditions provided the basis for this review.

Amanita phalloides poisoning causes severe liver damage which may be potentially fatal. Several treatments are available, but their effectiveness has not been systematically evaluated. We performed a systematic review to investigate the effect of the most commonly used therapies: N-acetylcysteine (NAC), benzylpenicillin (PEN), and silibinin (SIL) on patient outcomes. In addition, other factors contributing to patient outcomes are identified.
We searched MEDLINE and Embase for case series and case reports that described patient outcomes after poisoning with amanitin-containing Amanita mushrooms. We extracted clinical characteristics, treatment details, and outcomes. We used the liver item from the Poisoning Severity Score (PSS) to categorize intoxication severity.
We included 131 publications describing a total of 877 unique cases. The overall survival rate of all patients was 84%. Patients receiving only supportive care had a survival rate of 59%. The use of SIL or PEN was associated with a 90% (OR 6.40 [3.14-13.04]) and 89% (OR 5.24 [2.87-9.56]) survival rate, respectively. NAC/SIL combination therapy was associated with 85% survival rate (OR 3.85 [2.04, 7.25]). NAC/PEN/SIL treatment group had a survival rate of 76% (OR 2.11 [1.25, 3.57]). Due to the limited number of cases, the use of NAC alone could not be evaluated. Additional analyses in \'proven cases\' (amanitin detected), \'probable cases\' (mushroom identified by mycologist), and \'possible cases\' (neither amanitin detected nor mushroom identified) showed comparable results, but the results did not reach statistical significance. Transplantation-free survivors had significantly lower peak values of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total serum bilirubin (TSB), and international normalized ratio (INR) compared to liver transplantation survivors and patients with fatal outcomes. Higher peak PSS was associated with increased mortality.
Based on data available, no statistical differences could be observed for the effects of NAC, PEN or SIL in proven poisonings with amanitin-containing mushrooms. However, monotherapy with SIL or PEN and combination therapy with NAC/SIL appear to be associated with higher survival rates compared to supportive care alone. AST, ALT, TSB, and INR values are possible predictors of potentially fatal outcomes.

BACKGROUND: Amanita verna is one of the most harmful wild fungi in China. Amanita verna poisoning occurs every year, and the mortality is as high as 50%. However, its clinical manifestations are complex and diverse.
METHODS: In March 2019, three patients took a large amount of Amanita, and one of them received liver transplantation in Zhongshan hospital, Sun Yat-sen University. All patients had vomiting and diarrhea 8-12 h after eating wild mushrooms (Amanita). The patients were initially diagnosed with Amanita poisoning. One case (case 3) was complicated and diagnosed as mushroom poisoning (fatal Amanita), toxic hepatitis, acute liver failure, toxic encephalopathy, hemorrhagic colitis, toxic myocarditis, disseminated intravascular coagulation (DIC) and pregnancy. The general clinical data of all patients were recorded, who received early treatment such as hemodialysis, artificial liver plasma exchange, hormone shock and anti-infection. One case (case 1) recovered smoothly after liver transplantation, and the indexes of liver, kidney, coagulation function and infection were improved. The other two cases died of intracerebral hemorrhage.
CONCLUSIONS: Liver transplantation is an effective method for the treatment of acute liver failure caused by mushroom poisoning and can improve the survival rate of patients with toxic liver failure.

Amanita mushrooms are important for both human beings and ecosystems. Some members in this genus are valued edible species, whereas some others are extremely poisonous, and most species are ectomycorrhizal. Significant progress has been made in recent years in our understanding of the diversity, phylogeography and population genetics of Amanita mushrooms. A significant reason for the progress was due to the increasing application of molecular methods in the analyses. In this review, we summarize the researches in the diversity, phylogeography and population genetics of Amanita mushrooms, with the focus on advances over the past 20 years. We also discussed future research directions, including several unresolved topical issues.

Amanita phalloides poisoning with a high mortality is a serious health problem in the world. The typical clinical manifestations are usually characterized by the absence of any symptoms followed by severe gastrointestinal disorders and acute liver failure. Inhibition of RNA polymeraseII (RNAP II) activity, apoptosis, and oxidative stress are considered as the major mechanism of amatoxins intoxication. The current treatment measures mainly include prevention of amatoxins absorption, elimination of absorbed amatoxins, potential antidotes therapy, and liver transplantation. Nevertheless, there are no widely accepted treatment criteria for Amanita phalloides poisoning. This paper will focus on the treatment measures based on the previous studies and provide the currently available information for clinicians.

Mushroom is an important constituent of diet in many ethnic tribes in India. Ethnic Indian tribes are known to consume nearly 283 species of wild mushrooms out of 2000 species recorded world over. Although they are experts in distinguishing the poisonous from edible mushrooms, yet occasional cases of toxicity are reported due to accidental consumption of poisonous mushrooms. We report amanita like toxicity in a family after consumption of wild mushrooms resulting in fatal outcome.

BACKGROUND: Diagnosis and management of Amanita mushroom poisoning is a challenging problem for physicians across the United States. With 5902 mushroom exposures and two resultant deaths directly linked to Amanita ingestion in 2009, it is difficult for physicians to determine which patients are at risk for lethal toxicity. Identification of amatoxin poisoning can prove to be difficult due to delay in onset of symptoms and difficulty with identification of mushrooms. Consequently, it is difficult for the Emergency Physician to determine proper disposition. Further, treatment options are controversial.
OBJECTIVE: To review current data to help health care providers effectively identify and treat potentially deadly Amanita mushroom ingestions.
METHODS: We present two cases of Amanita mushroom ingestion in the northeastern United States treated with N-acetylcysteine, high-dose penicillin, cimetidine, and silibinin, a semi-purified fraction of milk thistle-derived silymarin, as part of their treatment regimen. The mushroom species was identified by a consultant as Amanita Ocreata.
CONCLUSIONS: We present the successful treatment of 2 patients who ingested what we believe to be an Amanita species never before identified in the northeastern United States.

BACKGROUND: In the Pacific Northwest a new pattern of mushroom ingestion has emerged, attributed to Amanita smithiana, in which renal failure has been the predominant manifestation.
METHODS: A 55-year-old male ate 3 raw wild mushrooms in a salad and had onset of severe nausea and vomiting within 6 hours. His vital signs were unremarkable. His labs were significant for a BUN of 14 mg/dL (5.0 mmol/L), and a creatinine of 1.0 mg/dL (88 umol/L), transaminases were elevated with an AST of 56 U/L (nl 9-40) and an ALT of 131 U/L (nl 14-72). Treatment was initiated with N-acetyl cysteine, penicillin, and milk thistle extract on the presumption that this was an amanitin-toxin containing mushroom. He developed acute renal failure that was not responsive to our treatment. Dialysis started on day 4 with a creatinine of 6.5 mg/dL, which peaked on day 7 at 10.2 mg/dL. We were able to obtain a positive mushroom identification by a mycologist as Amanita smithiana. The patient was discharged from the hospital for outpatient dialysis on day 10 and dialysis catheter was removed 39 days after ingestion with a creatinine of 1.4 mg/dL (123.8 umol/L).
CONCLUSIONS: Amanita smithiana mushroom poisoning presents within 6 hours of ingestion with GI toxicity, and develops delayed onset of renal insufficiency over the first 1 to 4 days. The early hospitalization of this case allowed a profile of the onset of liver and renal injury. Mild elevation of hepatic transaminases occurred on presentation and peaked 24 hours after the ingestion. Renal injury was detected 1 day after presentation, and progressed to require hemodialysis by 4 days postingestion. This pattern of delayed-onset renal toxic mushroom ingestion is emerging among mushroom ingestions in Western North America.

BACKGROUND: The potential benefit of silymarin (special extract from the fruits of Silybum marianum) in the treatment of liver diseases remains a controversial issue.
METHODS: For this systematic review electronic databases identified 65 papers for the search terms silymarin, silibinin, silicristin or milk thistle and clinical trial. Only 19 complied with the criteria\'double-\' or \'single-blind\'. These publications were analysed from a clinical point of view and meta-analytic calculations were performed.
RESULTS: The clinical evidence ofa therapeutic effect of silymarin in toxic liver diseases is scarce. There is no evidence of a favourable influence on the evolution of viral hepatitis, particularly hepatitis C. In alcoholic liver disease, comparing with placebo, aspartate aminotransferase was reduced in the silymarin-treated groups (p = 0.01) while alkaline phosphatase was not. In liver cirrhosis, mostly alcoholic, total mortality was 16.1% with silymarin vs. 20.5% with placebo (n.s.); liver-related mortality was 10.0% with silymarin vs. 17.3% with placebo(p = 0.01).
CONCLUSIONS: Based on the available clinical evidence it can be concluded - concerning possible risks /probable benefits - that it is reasonable to employ silymarin as a supportive element in the therapy of Amanita phalloides poisoning but also (alcoholic and grade Child \'A\') liver cirrhosis. A consistent research programme, consolidating existing evidence and exploring new potential uses,would be very welcome.

An analysis of patients with mushroom poisoning hospitalized in the Clinic of Toxicology in Cracow revealed that only a small percentage of cases had been caused by the death cap Amanita phalloides (Vaill. ex Fr.) Secr. The most important factors contributing to intoxication are confusion of toxic mushrooms with edible species, and non-specific mushroom poisoning. The genus Amanita has a global distribution and is one of the most well-known genera of macrofungi. Active toxins present in the panther cap (A. pantherina) (DC ex Fr.) Secr are ibotenic acid and muscimol, which are rapidly absorbed from the gastrointestinal tract. It is likely that other substances also participate in the psychotropic effects. Five frayed panther cap fruiting bodies were eaten by mistake by two persons (27 and 47 years of age). Symptoms onset occurred after 120 min with central nervous system (CNS) depression, ataxia, waxing and waning obtundation, religious hallucinations and hyperkinetic behaviour. In the present case, successful general symptomatic treatment was administered, which consisted of controlling the nervous symptoms and stabilizing the electrolyte balance. The poisoning regressed with no organ complications.