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.

Successful treatment of a child with fulminant liver failure and coma due to Amanita phalloides poisoning using urgent liver transplantation.

Intoxication due to eating wild mushrooms presents with a variety of signs, ranging from mild diarrhea to severe organ failure. We present the case of an 11-year-old boy with fulminant liver failure and hepatic coma due to Amanita phalloides poisoning treated with an urgent pediatric orthotopic liver transplantation. Successful treatment of patients with fulminant liver failure and hepatic coma caused by Amanita phalloides poisoning is possible using urgent orthotopic liver transplantation when conservative medical treatment modalities are ineffective.

[Liver albumin dialysis (MARS)--treatment of choice in Amanita phalloides poisoning?]. / Dializa albuminowa watroby (MARS)--leczenie z wyboru w ciezkim zatruciu muchomorem sromotnikowym?

UNLABELLED: Amanita phalloides is a direct life-threatening poisoning because of acute multiorgan failure. Urgent liver transplantation (LTx) is the last chance to save patient's life in severe cases. In many cases of mushroom poisoning the patient dies because of unavailability of a liver graft. Liver albumin dialysis (MARS) is a promising treatment to bridge the patient to LTx or stabilize his or her condition until spontaneous liver regeneration occurs. CASE REPORT: Four family members (father, mother and two sons) were eating self-collected mushrooms (Russula vesca). Typically for the Amanita phalloides poisoning, the first symptoms appeared in all persons more than 12 hours after mushroom ingestion. Because they did not improve, the whole family was admitted to the Regional Hospital in Ketrzyn (24 hours after mushroom ingestion). Mycological examination of gastric washings was positive only in the mother, in whom the Amanita phalloides spores were found. During the first 48 hours of poisoning the biochemical indexes of liver injury were observed in all persons. The whole family members were sent to centers where liver albumin dialysis could be performed: the mother was admitted to the Department of Nephrology and Dialysis Therapy in Olsztyn, the father and the first son were admitted to the Clinical Toxicology Department in Krak6w, and the second son was admitted to the Department of Internal Medicine and Acute Poisonings in Gdansk. Three albumin dialysis procedures were performed in the case of mother with complete liver recovery. After the first liver albumin dialysis, the father of the family was disqualified from the following procedures because of severe coagulation disturbances (GI bleeding), and died the fourth day after mushroom ingestion. The first son fulfilled the King's College criteria and was accepted for high urgency liver transplantation. After two albumin dialysis procedures had been able and the patient was urgently sent to the Department of General and Transplantation Surgery in Szczecin, where liver transplantation was successfully performed. The second son was treated conservatively with improvement of general condition and biochemical indexes and no albumin dialysis procedure was necessary. CONCLUSION: Liver albumin dialysis may be effective in severe Amanita phalloides poisoning to stabilize the condition of a patient until spontaneous liver regeneration occurs or as a bridge to LTx. In cases of a family poisoning, proper coordination and cooperation among toxicology departments and transplant centers is required.

Molecular adsorbent recirculating system--MARS as a bridge to liver transplantation in amanita phalloides intoxication.

UNLABELLED: A case of a 46-year-old female intoxicated with Amanita phalloides was presented. Since constant deterioration of her liver function she was put on the waiting list for urgent liver transplantation. To improve her clinical condition two sessions of Molecular Adsorbent Recirculating System were provided with transient good results. About 72 hours after the mushroom ingestion the patient had undergone liver transplantation. CONCLUSIONS: Despite good clinical condition the patients severely poisoned with Amanita phalloides should be placed on a waiting list for liver transplantation as early as possible. The Molecular Adsorbent Recirculating System should be introduced as soon as possible after Amanita phalloides intoxication. Albumin dialysis may be considered as a bridge for the liver transplantation in patients intoxicated with Amanita phalloides.

The 2-stage liver transplant: 3 clinical scenarios.

The main goal of 2-stage liver transplant is to provide time to obtain a new liver source. We describe our experience of 3 patients with 3 different clinical conditions. A 57-year-old man was retransplanted successfully with this technique due to hepatic artery thrombosis. However, a 38-year-old woman with fulminant toxic hepatitis and a 5-year-old-boy with abdominal trauma had poor outcome. This technique could serve as a rescue therapy for liver transplant patients who have toxic liver syndrome or abdominal trauma. These patients required intensive support during long anhepatic states. The transplant team should decide early whether to use this technique before irreversible conditions develop.

Amanita poisoning: treatment and the role of liver transplantation.

Fatal mushroom poisoning has long been recognized as a major health problem in western Europe and more recently in the United States. The majority of deaths are attributable to the genus Amanita. Amanita phalloides (death cap) has been found with increasing frequency across the United States and presents a significant health hazard in this country to those who pick and consume wild mushrooms. This article discusses the pharmacologic basis and clinical manifestations of Amanita intoxication. It outlines the rationale of various treatment modalities and, from these, summarizes a protocol that the authors believe will be useful to the clinician. In addition, two patients are presented who underwent successful orthotopic liver transplantation for fulminant hepatic failure secondary to Amanita poisoning. The role of liver transplantation both acutely and as treatment for chronic active hepatitis secondary to severe intoxication is discussed.

Liver transplantation for severe Amanita phalloides mushroom poisoning.

Amanita phalloides mushroom poisoning is an increasingly common and potentially lethal problem for which liver transplantation offers definitive therapy in selected patients. When significant liver dysfunction appears, early transfer to a liver transplant center is important to identify appropriate candidates and to begin the search for a donor organ. The clinical course of five severely poisoned patients, four of whom underwent liver transplantation, is reviewed. Indications for transplantation included primarily a markedly prolonged prothrombin time that was only partially correctable and a constellation of findings including metabolic acidosis, hypoglycemia, hypofibrinogenemia, and increased serum ammonia, following a marked elevation in serum aminotransferase levels. Unlike viral fulminant hepatic failure, grade III or IV hepatic encephalopathy, marked elevation of the serum bilirubin level, and azotemia were not indications for transplantation. Resected livers demonstrated hepatocyte viability of 0% to 30%. Manifestations of Amanita poisoning complicating preoperative and/or postoperative care included severe diarrhea, gastrointestinal hemorrhage, hypophosphatemia, bowel edema, and marrow suppression with lymphopenia, thrombocytopenia, and neutropenia. All five patients are well 1 year later. This largest experience with liver transplantation for Amanita poisoning further defines the early clinical and laboratory indications for, and the unique complicating features of, transplantation in this setting.

Morphology of hepatic stellate cells in patients with fulminant or subfulminant hepatitis requiring liver transplantation.

Hepatic stellate cells were studied by immuno-cytochemistry with anti smooth muscle alpha-actin antibody (an activation marker for these cells) and electron microscopy, in eleven patients transplanted for fulminant or subfulminant hepatitis. Numerous smooth muscle alpha-actin positive cells were found in necrotic areas. In both fulminant and subfulminant hepatitis, hepatic stellate cells appeared enlarged, often irregular, with spikes. There were numerous signs of activation and many contained numerous small lipid droplets. In the cases of fulminant hepatitis, hepatic stellate cells presented, at times, some subcellular damage. Hepatic stellate cells processes, often in several layers, displayed numerous cytoplasmic microfilaments with conspicuous dense plaques below the plasma membrane. Hepatic stellate cells were never surrounded by a basement membrane. The extracellular matrix was loose and granulofibrillar. In areas of multiacinar nodules (in cases of map-like pattern), hepatic stellate cells were grossly normal. These results are in agreement with in vitro data showing that acutely damaged hepatocytes activate hepatic stellate cells but do not fully transform them into myofibroblasts.

[Indications for liver transplantation in severe amanita phalloides mushroom poisoning]. / Indikationsstellung zur Lebertransplantation bei schwerer Knollenblätterpilzvergiftung.

The clinical course of 12 patients with mushroom poisoning was evaluated in order to define the parameters considered to be relevant to the indication for liver transplantation. Eight patients recovered under conservative therapy; one patient died due to pre-existing, concomitant cardiopulmonary disease. In three patients transplantations had to be performed because of severe liver failure. On admission, the transplanted patients had a decreased Quick's test score and factor V value (< 10%). The peak of liver enzymes, serum bilirubin, serum creatinine, partial thromboplastin time and azotemia were not of any prognostic value. Main indications for liver transplantation were a very low initial Quick's test score and factor V value (both < 10%) and their inadequate response under substitution therapy. The development of encephalopathy and renal failure were further parameters indicating poor prognosis.

[Orthotopic liver transplantation for severe amanita phalloides poisoning]. / Transplantation orthotopique du foie pour intoxication grave par amanite phalloïde.

Forty-eight hours after a women was poisoned by ingesting Amanita phalloides mushrooms, she developed fulminant hepatic failure with collapse, pH 7.24, lactic acidosis 7.6 mmol/l, hypoglycaemia 3.5 mmol/l, anuria and stage IV coma requiring tracheal intubation and mechanical ventilation. Transaminase level was up to 8,000 UI/l. Prothrombin and factor V levels were below 10 percent, with an APT time of 86 s versus a 29 s control time. Twenty-four hours after her admission, the patient underwent orthotopic liver transplantation. The postoperative period was uneventful, with return to consciousness and rapid normalization of hepatic biochemistry values, without signs of acute rejection. This 10th published case of orthotopic liver transplantation for Amanita phalloides poisoning with acute hepatic necrosis confirms that this type of treatment must be systematically envisaged in all such cases.

[Two different outcomes after Death Cap mushroom intoxication]. / To forskellige forløb af forgiftning med grøn fluesvamp.

Death Cap is one of the most lethal mushrooms in Denmark and may be mistaken for a non-toxic Asian mushroom. We report on two accidental cases admitted 12 and 17 hours after ingestion presenting with gastroenteritis and decline in liver function. The patient who arrived after 12 hours responded well to intensive treatment of liver failure and was discharged after 18 days. The other patient deteriorated in spite of intensive treatment and underwent liver transplantation. She was later discharged. Early diagnosis and treatment is essential.

Successful liver transplantation after 21 days of hepatic coma.

A 52-year-old women was treated after ingestion of different wild mushrooms. The case demonstrates that successful liver transplantation with full recovery of brain functions is possible even after 3 weeks of persisting severe hepatic encephalopathy.

Urgent liver transplantation for Amanita phalloides poisoning.

Amanita phalloides is a deadly wild mushroom causing severe damage in man ranging from diarrhea to organ dysfunction. If not treated, mortality is as high as 80%. Treatment includes supportive measures, inactivation of the toxin and if liver failure occurs liver transplantation. The indications for transplantation are debatable.

[Amanita poisoning--comparison of silibinin with a combination of silibinin and penicillin]. / Knollenblätterpilzvergiftung. Silibinin und Kombination von Silibinin und Penicillin im Vergleich.

BACKGROUND AND AIMS: Current treatment of amatoxin poisoning includes the administration of silibinin and penicillin in combination or silibinin alone. The aim of this study was to compare both therapeutic regimes. PATIENTS AND METHODS: Of 604 patients with the suspected diagnosis of amatoxin poisoning 367 were retrospectively analysed: 118 patients had received silibinin alone and 249 patients silibinin in combination with penicillin. Logistic regression analyses were applied to investigate the efficacy of both therapeutic regimens by comparing death and liver transplantation rates. A potentially independent effect on outcome of age, sex, year of treatment, latency period of symptoms and start of silibinin therapy was taken into account. RESULTS: In the group who had received the combination of silibinin and penicillin 8.8% died or underwent liver transplantation compared to 5.1% in the group of those who had received silibinin alone. The risk of death or organ transplantation was thus reduced by nearly 40% in the latter group (adjusted odds ratio: 0.58; 95% CI: 0.21-1.57; p=0.28). A longer latency period (< or =12h vs. >12h) was associated with a significant reduction of this risk (adjusted OR.: 6.10; 95% CI:1.77-21.3; p=0.004). A later start of silibinin therapy (>24h vs. < or = 24h) was associated with a tendency toward an increased frequency of death or organ transplantation (adjusted OR.: 3.0; 95% CI: 0.96-9.20; p=0.059). CONCLUSIONS: A lower death and transplantation rate was observed in the silibinin treatment group than in group treated with silibinin combined with penicillin. However, this difference was not statistically significant. The high risk ratio relating to the time-dependent effect of silibinin suggests its efficaciousness in the treatment of amatoxin poisoning. The latency period was assessed as an independent prognostic factor.

Mushroom poisoning: the role of orthotopic liver transplantation.

Mushroom poisoning, mycetismus, is a well-recognized cause of fulminant hepatic failure in Western Europe and is increasingly seen in the United States. We present a case of fulminant hepatic failure secondary to mushroom poisoning treated successfully with an orthotopic liver transplant.

Liver transplantation in mushroom poisoning.

Liver transplantation plays an important role in the treatment of patients with fulminant hepatic failure (FHF). Early determination of prognosis in cases of FHF is important to allow prompt decision-making regarding the need for liver transplantation. Mushroom poisoning is a rare cause of FHF, and as a result, prognostic criteria are not well recognized. It appears that the severity of coagulopathy and encephalopathy predicts a poor outcome, whereas the degree of bilirubin elevation may not. We present a case of FHF related to mushroom poisoning that required liver transplantation. The clinical presentation, medical management, and prognostic criteria in mushroom poisoning are discussed.

Treatment of amatoxin poisoning: 20-year retrospective analysis.

BACKGROUND: Amatoxin poisoning is a medical emergency characterized by a long incubation time lag, gastrointestinal and hepatotoxic phases, coma, and death. This mushroom intoxication is ascribed to 35 amatoxin-containing species belonging to three genera: Amanita, Galerina, and Lepiota. The major amatoxins, the alpha-, beta-, and gamma-amanitins, are bicyclic octapeptide derivatives that damage the liver and kidney via irreversible binding to RNA polymerase II. METHODS: The mycology and clinical syndrome of amatoxin poisoning are reviewed. Clinical data from 2108 hospitalized amatoxin poisoning exposures as reported in the medical literature from North America and Europe over the last 20 years were compiled. Preliminary medical care, supportive measures, specific treatments used singly or in combination, and liver transplantation were characterized. Specific treatments consisted of detoxication procedures (e.g., toxin removal from bile and urine, and extracorporeal purification) and administration of drugs. Chemotherapy included benzylpenicillin or other beta-lactam antibiotics, silymarin complex, thioctic acid, antioxidant drugs, hormones and steroids administered singly, or more usually, in combination. Supportive measures alone and 10 specific treatment regimens were analyzed relative to mortality. RESULTS: Benzylpenicillin (Penicillin G) alone and in association was the mostfrequently utilized chemotherapy but showed little efficacy. No benefit was found for the use of thioctic acid or steroids. Chi-square statistical comparison of survivors and dead vs. treated individuals supported silybin, administered either as mono-chemotherapy or in drug combination and N-acetylcysteine as mono-chemotherapy as the most effective therapeutic modes. Future clinical research should focus on confirming the efficacy of silybin, N-acetylcysteine, and detoxication procedures.