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At least 19 recordsLinked to original sources
PubMed1997

[Amanita pantherina and Amanita muscaria poisonings--pathogenesis, symptoms and treatment].

Amanita pantherina and Amanita muscaria are commonly occurring mushrooms in Polish forests. They contain ibotenic acid and muscimol: the substances reacting with neurotransmitter receptors in central nervous system. The ingestion of these mushrooms produces a distinctive syndrome consisting of alternating phase of drowsiness and agitation with hallucinations, and sometimes with convulsions. The diagnosis of Amanita pantherina or Amanita muscaria poisoning is established by means of mycologic investigation of gastric lavage. The treatment is only symptomatic, and the prognosis is usually good.

Amanita↗
PubMed1998

[Determination of toxic peptides in Amanita virosa and Amanita verna].

The toxic peptides in Amanita virosa and Amanita verna from various region were analyzed by a reversed-phase high-performance liquid chromatography. It is showed that there were great differences in the concentrations of toxic peptides between species and strains of A. virosa and A. verna.

Amanita↗
PubMedDate not supplied

Toxic metabolites of Amanita pantherina, A. cothurnata, A. muscaria and other Amanita species.

Forty-seven specimens representing 35 species or varieties of Amanita were examined for the presence of ibotenic acid, muscimol, stizolobic acid, stizolobinic acid, aminohexadienoic acid and chlorocrotylglycine. In addition, crude extracts of A. muscaria were examined chromatographically for the presence of methyltetrahydrocarboline carboxylic acid (MTC). Ibotenic acid and muscimol were found in clearly detectable concentrations in extracts of A. cothurnata, all specimens of A. muscaria, all specimens of A. pantherina and in lower concentrations in A. gemmata. Stizolobic acid and stizobinic acid were found in detectable concentrations in one variety of A. muscaria, in all specimens of A. pantherina and in trace levels after additional purification of the extracts in A. gemmata and in the remaining specimens of A. muscaria. Aminohexadienoic acid and chlorocrotylglycine were detected only in crude extracts of A. smithiana. MTC could not be detected in crude extracts of A. muscaria. Crystalline ibotenic acid (820 mg) was isolated from 17 kg of a specimen of A. pantherina collected in western Washington State.

Agaricales↗
PubMed1988

High-performance liquid chromatographic method for the determination of alpha-amanitin and phalloidin in human plasma using the column-switching technique and its application in suspected cases of poisoning by the green species of amanita mushroom (Amanita phalloides).

A reversed-phase high-performance liquid chromatographic assay has been developed for the simultaneous determination of alpha-amanitin and phalloidin in human plasma. The procedure is based on the enrichment of the toxins on a pre-column, followed by the transfer of both compounds in a foreflush mode to the analytical column. alpha-Amanitin and phalloidin can be quantified reliably down to a minimum concentration of 10 ng/ml in plasma (relative standard deviation less than 10%). An alternative method is recommended for hepatic coma patients.

Agaricales↗
PubMed1994

Amanita poisoning during the second trimester of pregnancy. A case report and a review of the literature.

Amanita phalloides-type mushroom poisoning is well recognized as causing acute liver injury and often death. Less is known, however, of whether maternal Amanita poisoning is associated with fetal damage or not. In August 1991 four members of a family were hospitalized with food intoxication caused by Amanita phalloides and Amanita verna. One of them died from hepatic and renal failure. The survivors included a 26-year-old woman in the 23rd week of pregnancy. Her clinical symptoms and blood chemistry data (lowest prothrombin activity 23%) indicated intoxication of medium severity. The management consisted of i.v. hydration, forced diuresis, and administration of silibinin, high-dose penicillin, thioctic acid, hydrocortisone, vitamin K, and fresh frozen plasma. Sonographic and obstetric controls failed to show any fetal abnormalities in the acute phase of poisoning. In the 38th week of pregnancy she gave birth to a healthy baby, who has subsequently undergone an undisturbed development. This observation indicated that severe fetal damage did not occur in maternal Amanita poisoning in the second trimester of pregnancy. Thus, at least from the second trimester on, maternal Amanita poisoning is not necessarily an indication for induced abortion.

Adolescent↗
PubMed2003

Effects of Amanita phalloides toxins on insulin release: in vivo and in vitro studies.

The clinical picture of Amanita phalloides poisoning includes hypoglycaemia, usually related to hepatic damage. In fact, Amanita toxins induce hepatic glycogen depletion in humans and animals. However, in animals morphological changes of pancreatic beta cells are reported, suggesting that an alteration of insulin secretion might be involved in the pathogenesis of hypoglycaemia. Therefore, we determined fasting glucose, insulin and C-peptide levels in ten patients intoxicated by Amanita phalloides and in ten control subjects. Fasting blood samples were drawn on 3 consecutive days, beginning 48-72 h after mushroom ingestion, and glucose, insulin and C-peptide concentrations were determined by routine methods. Serum glucose concentrations did not differ between poisoned subjects and controls, whereas insulin and C-peptide concentrations were significantly higher in poisoned subjects ( P<0.01), with a significant positive correlation ( R=0.97, P<0.001). We also evaluated the effects of alpha-amanitin, the main amatoxin, on in vitro insulin release. Rat islets were incubated with 5 and 50 mg/l alpha-amanitin, in the presence or absence of 5.6 mM glucose. In another protocol, islets were preincubated for 2 h with 5 and 50 mg/l alpha-amanitin in medium containing 5.6 mM glucose. After lavage, islets were incubated with increasing glucose (2.8-22.0 mM) to evaluate insulin release. In vitro, both concentrations of toxin induced insulin release (5 mg/l P<0.02, 50 mg/l P<0.01 vs controls), in the presence of 5.6 mM glucose. Islets preincubated with 5 mg/l alpha-amanitin showed a pattern of glucose-stimulated insulin release similar to controls, whereas islets preincubated with 50 mg/l alpha-amanitin showed an increased basal release with a reduced response to glucose stimulation. These observations show that Amanita toxins might play a role in the clinical context of Amanita poisoning. We demonstrate, for the first time, that alpha-amanitin induces insulin release and may exert a cytotoxic effect on beta cells.

Adult↗