CLIF-OF >9 predicts poor outcome in patients with Amanita phalloides poisoning.

PURPOSE: Amanita phalloides poisoning with high mortality is rare but serious. The aim of this study is to identify the risk indicators of death in patients with Amanita phalloides poisoning and a good score tool to predict prognosis. METHODS: In this respective study (1/2009-12/2018), the patients (n = 105) with Amanita phalloides poisoning from two hospitals of China Medical University who met the inclusion/exclusion criteria were included. The laboratory markers and the clinical scoring systems including Child-Turcotte-Pugh (CTP), Sequential organ failure assessment (SOFA), Liver injury and Failure evaluation (LiFe), Chronic liver failure-organ failure score system (CLIF-OF), King's College criteria (KCH criteria), Model for end-stage liver disease (MELD) and Platelet-bilirubin-albumin (PALBI) within 24 h of admission to the two hospitals were analyzed and area under the curve (AUC) analyses were also performed regarding the prediction of death. RESULTS: The data analysis indicated that high international normalized ratio (INR) (>3.6, AUC = 0.941) and plasma ammonia (>95.1 µmol/L, AUC = 0.805) were closely associated with mortality after multivariate logistic regression. CLIF-OF (>9) within 24 h with really good diagnostic accuracy (>90%) significantly outperformed the other scores in predicting mortality. CONCLUSION: CLIF-OF (>9) within 24 h of admission is considered as a satisfactory and practical tool to predict a poor outcome of Amanita phalloides poisoning.

Amanita phalloides intoxication: mechanism of toxicity, clinical manifestations and therapeutic approaches.

Ingestion of Amanita phalloides is the most common cause of fatal mushroom poisoning. The clinical picture of intoxication varies from mild subclinical manifestation to lethal fulminant course with the development of acute liver failure. Early diagnosis of Amanita phalloides poisoning is crucial for the outcome but i tis difficult because it is often mistaken as gastroenteritis or due to other mushroom poisoning. The diagnosis is based on the history of recent mushroom ingestion followed by gastrointestinal symptoms, typical time course and laboratory markers and is proven with mycological examination or toxicological examination. Specific treatment consists of detoxification procedures, supportive measures, administration of drugs and therapy in the specialized intensive care unit in the case of acute liver failure. In selected patients with acute liver failure urgent liver transplantation is the only life-saving option.

Significance and outcome of living-donor liver transplantation in acute mushroom intoxication.

INTRODUCTION: Mushroom intoxication (MT) can lead to acute liver injury which may result in Mushroom intoxication-related liver failure (M-ALF) requiring liver transplantation (LT). In the present study, we want to share the experience of our institute regarding living-donor LT (LDLT) due to mushroom poisoning. AIM: The aim of this study is to identify the predictors of poor prognosis in patients with ALF secondary to mushroom intoxication requiring LDLT. MATERIALS AND METHODS: All patients with MT between 2008 and 2016 were evaluated. Demographics, symptoms, interval between symptoms and admission to our institute, laboratory data, model for end-stage liver disease (MELD)/pediatric end-stage liver disease (PELD) scores, clinical course, and outcomes of supportive therapy and LT were evaluated. There were two groups in the study: Group A = responsive to supportive therapy (n = 9) versus Group B = unresponsive to supportive therapy (n = 9). RESULTS: During the study, a total of 18 patients were admitted with M-ALF. Twelve (66.7%) of them were female, and the mean age was 39.9 ± 18.2 years. All of the nine patients in Group A fully recovered with supportive therapy. In Group B, one patient died during waiting period for LT and 8 patients received LDLT LDLT. Three of the eight patients who were transplanted died in the postoperative early period within postoperative 5 days. The patients in Group B had significantly higher MELD/PELD scores and encephalopathy rate than in Group A (P < 0.05). International normalized ratio (INR), bilirubin, ammonium levels, and platelet count were significantly different between groups (P < 0.05). The patients in Group B had significantly longer interval before admission to our institute (P < 0.05). CONCLUSION: The presence of encephalopathy, higher MELD/PELD, INR, bilirubin, ammonium levels, and lower platelet count was related to poor prognosis in MT. LDLT provides a good therapeutic option in patients with M-ALF. The time is a crucial factor in successful treatment of MT. Early admission to a tertiary referral center with expertise in LT results in a better prognosis and increased survival following M-ALF.

Features of Patients With Severe Hepatitis Due to Mushroom Poisoning and Factors Associated With Outcome.

BACKGROUND & AIMS: Acute liver failure after ingestion of toxic mushrooms is a significant medical problem. Most exposures to toxic mushrooms produce no symptoms or only mild gastroenteritis, but some lead to severe hepatic necrosis and fulminant hepatic failure requiring liver transplantation. We aimed to assess mortality from mushroom poisoning and identify variables associated with survival and liver transplantation. METHODS: We collected information from 27 patients (13 male; median age, 47 years) admitted to the emergency department within 24 hours of ingesting wild mushrooms. They developed severe liver injury (serum levels of transaminases greater than 400 IU/L) and were treated with activated charcoal and N-acetylcysteine at a tertiary medical center in San Francisco, California from January 1997 through December 2014. Viral hepatitis, autoimmune liver disease, acetaminophen, salicylate toxicity, and chronic liver diseases were ruled out for all patients. We analyzed patient demographics, time since ingestion, presenting symptoms, laboratory values, and therapies administered. A good outcome was defined as survival without need for liver transplant. A poor outcome was defined as death or liver transplant. Positive predictive values were calculated, and the χ2 test was used to analyze dichotomous variables. RESULTS: Liver injury was attributed to ingestion of Amanita phalloides in 24 patients and Amanita ocreata in 3 patients. Twenty-four of the patients ingested mushrooms with meals and 3 patients for hallucinogenic purpose. At 24-48 hours after ingestion, all patients had serum levels of alanine aminotransferase ranging from 554 to 4546 IU/L (median, 2185 IU/L). Acute renal impairment developed in 5 patients. Twenty-three patients survived without liver transplantation, and 4 patients had poor outcomes (1 woman underwent liver transplantation on day 20 after mushroom ingestion, and 3 women died of hepatic failure). Of the 23 patients with peak levels of total bilirubin of 2 mg/dL or more during hospitalization, only 4 had a poor outcome. Peak serum level of aspartate aminotransferase less than 4000 IU/L, peak international normalized ratio less than 2, and a value of serum factor V greater than 30% identified patients with good outcomes with 100% positive predictive value; if these peak values were used as a cutoff, 10 of 27 patients (37%), 7 of 27 patients (26%), and 6 of 12 patients (50%), respectively, could have avoided transfer to a transplant center. CONCLUSIONS: In an analysis of 27 patients with hepatocellular damage due to mushroom (Amanita) poisoning and peak levels of total bilirubin greater than 2 mg/dL, the probability of liver transplantation or death is 17%, fulfilling Hy's law. Patients with peak levels of aspartate aminotransferase less than 4000 IU/L can be monitored in a local hospital, whereas patients with higher levels should be transferred to liver transplant centers. Women and older patients were more likely to have a poor outcome than men and younger patients.

A universal method for the identification of genes encoding amatoxins and phallotoxins in poisonous mushrooms

Background: As the currently known diagnostic DNA targets amplified in the PCR assays for detection of poisonous mushrooms have their counterparts in edible species, there is a need to design PCR primers specific to the genes encoding amanitins and phallotoxins, which occur only in poisonous mushrooms. Objective: The aim of the study was testing of PCR-based method for detection of all genes encoding hepatotoxic cyclic peptides - amanitins and phallotoxins present in the most dangerous poisonous mushrooms. Material and Methods: Degenerate primers in the PCR were designed on the basis of amanitins (n=13) and phallotoxins (n=5) genes in 18 species of poisonous mushrooms deposited to Genbank of the National Center for Biotechnology Information. Results: The specificity of the PCR assays was confirmed against 9 species of edible mushrooms, death cap - Amanita phalloides and panther cap - Amanita pantherina. Conclusions: Designed two couples of PCR-primers specific to amanitins and phallotoxins genes can be recommended for detection of Amanita phalloides and other mushroom species producing hepatotoxic cyclic peptides - amanitins and phallotoxins.

Acute liver injury and acute liver failure from mushroom poisoning in North America.

BACKGROUND & AIMS: Published estimates of survival associated with mushroom (amatoxin)-induced acute liver failure (ALF) and injury (ALI) with and without liver transplant (LT) are highly variable. We aimed to determine the 21-day survival associated with amatoxin-induced ALI (A-ALI) and ALF (A-ALF) and review use of targeted therapies. METHODS: Cohort study of all A-ALI/A-ALF patients enrolled in the US ALFSG registry between 01/1998 and 12/2014. RESULTS: Of the 2224 subjects in the registry, 18 (0.8%) had A-ALF (n = 13) or A-ALI (n = 5). At admission, ALF patients had higher lactate levels (5.2 vs. 2.2 mm, P = 0.06) compared to ALI patients, but INR (2.8 vs. 2.2), bilirubin (87 vs. 26 µm) and MELD scores (28 vs. 24) were similar (P > 0.2 for all). Of the 13 patients with ALF, six survived without LT (46%), five survived with LT (39%) and two died without LT (15%). Of the five patients with ALI, four (80%) recovered and one (20%) survived post-LT. Comparing those who died/received LT (non-spontaneous survivors [NSS]) with spontaneous survivors (SS), N-acetylcysteine was used in nearly all patients (NSS 88% vs. SS 80%); whereas, silibinin (25% vs. 50%), penicillin (50% vs. 25%) and nasobiliary drainage (0 vs. 10%) were used less frequently (P > 0.15 for all therapies). CONCLUSION: Patients with mushroom poisoning with ALI have favourable survival, while around half of those presenting with ALF may eventually require LT. Further study is needed to define optimal management (including the use of targeted therapies) to improve survival, particularly in the absence of LT.

Determination of amatoxins and phallotoxins in Amanita phalloides mushrooms from northeastern Portugal by HPLC-DAD-MS.

Amanita phalloides is a toxic mushroom responsible for the majority of deaths occurring after mushrooms ingestion, mainly due to amatoxins. In the present study the contents and distribution of the major amatoxins and phallotoxins in different tissues of A. phalloides from two different sites of Portugal were analyzed by liquid chromatography (LC) coupled to diode array (DAD) and mass spectrometry (MS) detection. The main toxins were separated by LC and its chemical structures confirmed by MS. α-Amanitin contents in caps, stipe and volva tissues were quantified by RP-HPLC. The results show that caps have the highest content of amatoxins, whereas the volva was richest in phallotoxins. Moreover variability in the toxins composition from different geographic sites was also observed. This study provides for the first time the content of toxins in A. phalloides from Portugal.

Amatoxin and phallotoxin concentration in Amanita phalloides spores and tissues.

Most of the fatal cases of mushroom poisoning are caused by Amanita phalloides. The amount of toxin in mushroom varies according to climate and environmental conditions. The aim of this study is to measure α-, ß-, and γ-amanitin with phalloidin and phallacidin toxin concentrations. Six pieces of A. phalloides mushrooms were gathered from a wooded area of Düzce, Turkey, on November 23, 2011. The mushrooms were broken into pieces as spores, mycelium, pileus, gills, stipe, and volva. α-, ß-, and γ-Amanitin with phalloidin and phallacidin were analyzed using reversed-phase high-performance liquid chromatography. As a mobile phase, 50 mM ammonium acetate + acetonitrile (90 + 10, v/v) was used with a flow rate of 1 mL/min. C18 reverse phase column (150 × 4.6 mm; 5 µm particle) was used. The least amount of γ-amanitin toxins was found at the mycelium. The other toxins found to be in the least amount turned out to be the ones at the spores. The maximum amounts of amatoxins and phallotoxin were found at gills and pileus, respectively. In this study, the amount of toxin in the spores of A. phalloides was published for the first time, and this study is pioneering to deal with the amount of toxin in mushrooms grown in Turkey.

A Case Study: What Doses of Amanita phalloides and Amatoxins Are Lethal to Humans?

There are few data estimating the human lethal dose of amatoxins or of the toxin level present in ingested raw poisonous mushrooms. Here, we present a patient who intentionally ingested several wild collected mushrooms to assess whether they were poisonous. Nearly 1 day after ingestion, during which the patient had nausea and vomiting, he presented at the emergency department. His transaminase levels started to increase starting from hour 48 and peaking at hour 72 (alanine aminotransferase 2496 IU/L; aspartate aminotransferase 1777 IU/L). A toxin analysis was carried out on the mushrooms that the patient said he had ingested. With reversed-phase high-performance liquid chromatography analysis, an uptake of approximately 21.3 mg amatoxin from nearly 50 g mushroom was calculated; it consisted of 11.9 mg alpha amanitin, 8.4 mg beta amanitin, and 1 mg gamma amanitin. In the urine sample taken on day 4, 2.7 ng/mL alpha amanitin and 1.25 ng/mL beta amanitin were found, and there was no gamma amanitin. Our findings suggest that the patient ingested approximately 0.32 mg/kg amatoxin, and fortunately recovered after serious hepatotoxicity developed.

Temporary left ventricular dysfunction in mushroom poisoning: report of three cases.

Mushroom poisoning can result in acute kidney injury and fulminant hepatic failure as well as gastrointestinal and neurological disorders. The effects of mushroom poisoning on cardiac functions have not been known well. Only a few case reports have been published to date (1-3). We report 3 patients out of 45 patients who were followed due to acute kidney injury and hepatic injury secondary to naturally growing mushroom ingestion between 2009 and 2012. These three cases suffered from transient impairment in cardiac systolic function in addition to other manifestations of mushroom poisoning.

Establishment and validation of a nomogram model for prediction of clinical outcomes in patients with amanita phalloides poisoning.

Amanita phalloides poisoning, renowned for its high mortality rates, is one of the most serious food safety issue in certain regions worldwide. Assessment of prognosis and development of more efficacious therapeutic strategies are critical importance for amanita phalloides poisoning patients. The aim of the study is to establish a nomogram to predict the clinical outcome of amanita phalloides poisoning patients based on the independent risk factor for prognosis. Herein, between January 2013 and September 2023, a cohort of 149 patients diagnosed with amanita phalloides poisoning was enrolled and randomly allocated into training and validation cohorts, comprising 102 and 47 patients, respectively. Multivariate logistic regression analysis was performed to identify the independent risk factors for morality of amanita phalloides poisoning patients in training cohort. Subsequently, a nomogram model was constructed to visually display the risk prediction model. The predictive accuracy of nomogram was verified by the validation cohort. The C index, the area under the receiver operating characteristic curve (AUC), and calibration plots were used to assessed the performance of nomogram. The clinical utility was evaluated by decision curve analysis (DCA). In the present study, the results showed that hepatic encephalopathy (HE), upper gastrointestinal bleeding (UGB), AST, and PT were the independent risk factors associated with the mortality of amantia phalloides poisoning patients. We constructed a new nomogram to evaluate the probability of death induced by amantia phalloides poisoning. The AUC for the prediction accuracy of the nomogram was 0.936 for the training cohort and 0.929 for the validation cohort. The calibration curves showed that the predicted probability matched the actual likelihood. The results of the DCA suggested that the nomogram has a good potential for clinical application. In summary, we developed a new nomogram to assess the probability of mortality for amanita phalloides poisoning patients. This nomogram might facilitate clinicians in making more efficacious treatment strategies for patients with amanita phalloides poisoning.

Effects of interrupting the enterohepatic circulation in amatoxin intoxications.

BACKGROUND: Interruption of the enterohepatic circulation is regarded as an effective way to treat patients with amatoxin poisoning. Nonetheless, its effectiveness has not yet been systematically evaluated. Therefore, we performed a systematic review to investigate the role of enterohepatic circulation on patient outcome and clinical laboratory values. We specifically sought to evaluate the effect of activated charcoal, which absorbs drugs and toxins in the gastrointestinal tract. METHODS: A previously established database with data extracted from case reports and series from literature, supplemented with recent publications, was used. Patient characteristics, outcome, and laboratory values were evaluated. RESULTS: We included 133 publications describing a total of 1,119 unique cases. Survival was 75 per cent in the control group (n = 452), whereas in the group treated with single or multiple doses of activated charcoal (n = 667) survival was 83 per cent (P < 0.001, odds ratio 1.89 [95 per cent confidence interval 1.40-2.56]). Furthermore, no difference in peak values of alanine aminotransferase and aspartate aminotransferase activities were observed, whereas peak values of total serum bilirubin concentration and international normalized ratio were statistically significantly reduced in patients treated with activated charcoal. DISCUSSION: The ability of activated charcoal to enhance the elimination of amatoxin through interruption of the enterohepatic circulation offers a potentially safe and inexpensive therapy for patients in the post-absorptive phase. LIMITATIONS: Limitations include the potential for publication bias, the lack of universal confirmation of amatoxin concentrations, and the inability to directly measure enterohepatic circulation of amatoxin. CONCLUSION: Treatment with activated charcoal in patients with amatoxin poisoning was associated with a greater chance of a successful outcome. Additionally, activated charcoal was associated with a reduction in markers of liver function, but not markers of liver injury.

The effects of CDP-choline treatment in Amanita phalloides mushroom toxicosis.

Amanita phalloides poisoning is known to be the most fatal case among mushroom poisoning cases. Its main mechanism of toxicity is that it leads to cell death by the irreversible binding of its toxins to the DNA-dependent RNA polymerase II enzyme. This study was planned to analyze the effects of the CDP-choline molecule on Amanita phalloides mushroom poisoning cases. The extract of the Amanita phalloides mushroom was taken and intraperitoneally administered to male Wistar Albino rats at a dose of 0.3 g/kg. In the experiment phase, the rats were divided into three groups of CDP-choline treatment according to the doses of 100 mg/kg, 250 mg/kg, and 500 mg/kg, and one control group was administered a 1 ml/kg dose of 0.9% isotonic NaCl solution. The treatments were then administered intraperitoneally at the 2nd hour, and at the 6th hour, the rats were sacrificed. The degree of damage in the liver and kidney tissues of the rats was evaluated histopathologically. It was concluded that CDP-choline reduced or prevented the damage that occurred in the liver significantly and dose-dependently in the toxicosis picture caused by Amanita phalloides, and it showed a tendency to lower or prevent the damage in the kidney, albeit not significantly.

Unexpected Amanita phalloides-Induced Hematotoxicity-Results from a Retrospective Study.

INTRODUCTION: Amanita phalloides poisoning is a serious health problem with a mortality rate of 10-40%. Poisonings are characterized by severe liver and kidney toxicity. The effect of Amanita phalloides poisonings on hematological parameters has not been systematically evaluated thus far. METHODS: Patients with suspected Amanita phalloides poisonings were retrospectively selected from the hospital database of the University Medical Center Groningen (UMCG). Medical data-including demographics; liver, kidney, and blood parameters; treatment; and outcomes-were collected. The severity of the poisoning was scored using the poison severity score. RESULTS: Twenty-eight patients were identified who were admitted to the UMCG with suspected Amanita phalloides poisoning between 1994 and 2022. A time-dependent decrease was observed for hemoglobin and hematocrit concentrations, leukocytes, and platelets. Six out of twenty-eight patients developed acute liver failure (ALF). Patients with ALF showed a higher increase in liver enzymes, international normalized ratios, and PSS compared to patients without ALF. Conversely, hemoglobin and platelet numbers were decreased even further in these patients. Three out of six patients with ALF died and one patient received a liver transplant. CONCLUSION: Our study shows that Amanita phalloides poisonings may be associated with hematotoxicity in patients. The quantification of hematological parameters is of relevance in intoxicated patients, especially in those with ALF.

Biodistribution of radiolabeled alpha-amanitin in mice: An Investigation.

Mushroom poisonings caused by Amanita phalloides are the leading cause of mushroom-related deaths worldwide. Alpha-Amanitin (α-AMA), a toxic substance present in these mushrooms, is responsible for the resulting hepatotoxicity and nephrotoxicity. The objective of our study was to determine the distribution of α-AMA in Balb/c mice by labeling with Iodine-131. Mice were injected with a toxic dose (1.4 mg/kg) of α-AMA labeled with Iodine-131. The mice were sacrificed at the 1st, 2nd, 4th, 8th, 24th, and 48th hours under anesthesia. The organs of the mice were removed, and their biodistribution was assessed in all experiments. The percent injected dose per gram (ID/g %) value for kidney, liver, lung, and heart tissues at 1st hour were 1.59 ± 0.07, 1.25 ± 0.33, 3.67 ± 0.80 and 1.07 ± 0.01 respectively. This study provides insights into the potential long-term effects of α-AMA accumulation in specific organs. Additionally, this study has generated essential data that can be used to demonstrate the impact of antidotes on the biological distribution of α-AMA in future toxicity models.

Unraveling Hematotoxicity of α-Amanitin in Cultured Hematopoietic Cells.

Amanita phalloides poisonings account for the majority of fatal mushroom poisonings. Recently, we identified hematotoxicity as a relevant aspect of Amanita poisonings. In this study, we investigated the effects of the main toxins of Amanita phalloides, α- and ß-amanitin, on hematopoietic cell viability in vitro. Hematopoietic cell lines were exposed to α-amanitin or ß-amanitin for up to 72 h with or without the pan-caspase inhibitor Z-VAD(OH)-FMK, antidotes N-acetylcysteine, silibinin, and benzylpenicillin, and organic anion-transporting polypeptide 1B3 (OATP1B3) inhibitors rifampicin and cyclosporin. Cell viability was established by trypan blue exclusion, annexin V staining, and a MTS assay. Caspase-3/7 activity was determined with Caspase-Glo assay, and cleaved caspase-3 was quantified by Western analysis. Cell number and colony-forming units were quantified after exposure to α-amanitin in primary CD34+ hematopoietic stem cells. In all cell lines, α-amanitin concentration-dependently decreased viability and mitochondrial activity. ß-Amanitin was less toxic, but still significantly reduced viability. α-Amanitin increased caspase-3/7 activity by 2.8-fold and cleaved caspase-3 by 2.3-fold. Z-VAD(OH)-FMK significantly reduced α-amanitin-induced toxicity. In CD34+ stem cells, α-amanitin decreased the number of colonies and cells. The antidotes and OATP1B3 inhibitors did not reverse α-amanitin-induced toxicity. In conclusion, α-amanitin induces apoptosis in hematopoietic cells via a caspase-dependent mechanism.

A comparison of the accuracy of mushroom identification applications using digital photographs.

OBJECTIVE: To compare the accuracy of three popular mushroom identification software applications in identifying mushrooms involved in exposures reported to the Victorian Poisons Information Centre and Royal Botanic Gardens Victoria. BACKGROUND: Over the past 10 years, an increasing number of software applications have been developed for use on smart phones and tablet devices to identify mushrooms. We have observed an increase in poisonings after incorrect identification of poisonous species as edible, using these applications. DESIGN: We compared the accuracy of three iPhone™ and Android™ mushroom identification applications: Picture Mushroom (Next Vision Limited©), Mushroom Identificator (Pierre Semedard©), and iNaturalist (iNaturalist, California Academy of Sciences©). Each app was tested independently by three researchers using digital photographs of 78 specimens sent to the Victorian Poisons Information Centre and Royal Botanic Gardens Victoria over a two-year period, 2020-2021. Mushroom identification was confirmed by an expert mycologist. For each app, individual and combined results were compared. RESULTS: Picture Mushroom was the most accurate of the three apps and correctly identified 49% (95% CI [0-100]) of specimens, compared with Mushroom Identificator (35% [15-56]) and iNaturalist (35% [0-76]). Picture Mushroom correctly identified 44% of poisonous mushrooms [0-95], compared with Mushroom Identificator (30% [1-58]) and iNaturalist (40% [0-84), but Mushroom Identificator identified more specimens of Amanita phalloides correctly (67%), compared to Picture Mushroom (60%) and iNaturalist (27%). Amanita phalloides was falsely identified, twice by Picture Mushroom and once by iNaturalist. CONCLUSIONS: Mushroom identification applications may be useful future tools to assist clinical toxicologists and the general public in the accurate identification of mushrooms species but, at present, are not reliable enough to exclude exposure to potentially poisonous mushrooms when used alone.

Acute Liver Injury From Mushroom Ingestion: A Timely Intervention in Mushroom Poisoning.

Mushroom poisoning, known as mycetism, represents a pressing health concern worldwide. Although the majority of mushroom ingestions are benign, select species like "Amanita phalloides" can induce catastrophic liver damage, culminating in acute liver failure. In this report, we detail a case involving a 35-year-old female who presented to the emergency department exhibiting symptoms of nausea, vomiting, abdominal pain, and palpitations merely six hours post-ingestion of "Amanita phalloides." Accurate identification of the specific mushroom species consumed proves challenging in over 90% of poisoning incidents, underscoring the necessity for clinical vigilance. While many mushroom exposures lead to mild gastrointestinal symptoms, recognizing the potential for severe outcomes is paramount for timely and effective intervention.

Malicious Mushrooms.

Accidental ingestion of the toxic Death Cap mushroom, and others of the Amantina species, can occur due to their physical similarities with commonly edible fungi. Production of certain toxins which prevent protein synthesis can lead to fulminant organ failure and death. Although treatment is mostly supportive due to a lack of specific antidote, early recognition can aid in meaningful recovery. Nonspecific symptoms are generally present early in the course and, therefore, high index of suspicion is required. We present 2 cases of suspected Amanita phalloides poisoning leading to acute liver injury; one leading to resolvement of symptoms and the other being fatal.

Cyclopeptide mushroom poisoning: A retrospective series of 204 patients.

Cyclopeptide mushroom poisoning is responsible for 90%-95% of deaths from macrofungi ingestion. The main objectives of this study are to describe cases of cyclopeptide mushroom poisoning and to determine risk factors that may influence the severity/mortality of poisoned patients. We included all cases of amatoxin toxicity reported to two French Poison Centers from 2013 through 2019. We compared the severity with the Poison Severity Score (PSS) and the outcomes of patients using simple logistic regression and multinomial logistic regression. We included 204 cases of amatoxin toxicity. More than three-quarters developed an increase in AST and/or ALT (78.1%), and over half developed a decrease in prothrombin ratio (<70%: 53%) and/or Factor V (<70%: 54%). One-third developed an acute renal injury (AKI). Twelve patients (5.9%) developed post-poisoning sequelae (persistent kidney injury more than 1 month after ingestion and liver transplant). Five patients (2.5%) received a liver transplant, and nine died (4.4%). The mean time to onset of digestive disorders was shorter in PSS2 and PSS3-4 patients (10.9 ± 3.9/11.3 ± 6.3 h) than in PSS1 patients (14 ± 6.5 h; p < 0.05). Patients who died or developed post-poisoning sequelae had more frequent cardiovascular comorbidities compared with recovered patients (60.0% versus 29.5%; p < 0.01).