Nicotinic acid treatment for Paralepistopsis acromelalga intoxication: assessment using magnetic resonance imaging.

CONTEXT: Paralepistopsis acromelalga, formerly known as Clitocybe acromelalga, is a rare poisonous mushroom. The mycotoxins in this mushroom cause symptoms resembling those of erythromelalgia; however, its pathogenesis remains unclear. In this report, a patient who received nicotinic acid treatment for P. acromelalga poisoning and radiological evaluation for erythromelalgia has been presented. Case detail: A 59-year-old woman was hospitalized for redness, swelling, and burning pain in her extremities that rendered difficulty in walking, and a diagnosis of P. acromelalga poisoning was made by detailed interview and mushroom identification. She was treated with intravenous nicotinic acid for 17 days followed by oral nicotinic acid amide for 2 months. She exhibited rapid symptomatic improvement and walked independently after 11 days of initial treatment. Initial MRI of her feet revealed toe-dominated subcutaneous thickening. After nicotinic acid treatment, those radiological findings improved dramatically. DISCUSSION: The subcutaneous thickening evident on MRI indicated P. acromelalga poisoning-induced erythromelalgia involved subcutaneous inflammatory edema. The typical duration of edema without treatment is more than a month. The improvement on MRI after nicotinic acid treatment indicated that the adequate vasodilation induced by nicotinic acid contributed to resolution of the symptoms. Nicotinic acid was associated with the improvement of the edematous changes caused by the P. acromelalga intoxication.

Assessment of emergency liver transplantation criteria in acute liver failure due to Amanita phalloides.

BACKGROUND AND AIMS: The emergency liver transplantation criteria for acute liver failure (ALF) due to Amanita phalloides (A. phalloides) intoxication are not consensual. The aims of this study were to evaluate the clinical outcomes, and to assess the accuracy of the current and specific criteria for emergency liver transplantation in predicting fatal outcome in ALF induced by A. phalloides. METHODS: Ten patients admitted with ALF induced by A. phalloides in a Gastroenterology Intensive Care Unit were studied. Indications for liver transplant were based on Clichy and/or King's College criteria. Specific criteria of Ganzert and Escudié were tested retrospectively. RESULTS: A. phalloides intoxication represented 11.6% of all admissions for ALF. Patients were admitted at a mean time of 60 ± 20.4 h after ingestion. Eight patients met the Clichy and/or King's College criteria for emergency liver transplantation, seven of these patients were listed for transplant and only six patients were transplanted. Four (40%) patients died in a mean time of 4.8 ± 0.74 days after ingestion. When applied retrospectively, Escudié's criteria showed 100% of accuracy for predicting fatal outcome, whereas, King's College, Clichy's and Ganzert's criteria had an accuracy of 90, 80 and 70%, respectively. A prothrombin index of less than 10% at day 3 after ingestion showed a positive predictive value of 100% and a negative predictive value of 60%. CONCLUSION: Escudié's criteria show the best accuracy for emergency liver transplant in ALF induced by A. phalloides. The assessment of these criteria at day 3 after ingestion shows a maximum positive predictive value, although with a decline in its negative predictive value.

[The assessment of albumin liver dialysis--MARS efficacy in the treatment of Amanita phalloides poisoning]. / Ocena skutecznosci albuminowej dializy watroby--MARS w terapii zatruc muchomorem sromotnikowym.

Fourteen patients were included to the albumin dialysis--MARS in the Clinic of Internal Medicine Geriatry and Clinical Toxicology in the years 2004-2006 because of acute intoxication with Amanita phalloides. The 26 procedures were done. Ten patients recovered, one was transplanted and three patients at the age from 68 to 79 (average 72.6) years died because of acute liver failure (21.4% cases). All deceased patients had significant higher plasma bilirubin level and INR in compare to other probants. The procedures of albumin dialysis caused significant lowering of blood glucose level, red blood cells and platelets, but without the need for intervention.

Causes of death in fulminant hepatic failure and relationship to quantitative histological assessment of parenchymal damage.

The clinical course and causes of death in 132 consecutive patients with fulminant hepatic failure and grade III or IV encephalopathy have been reviewed. 105 patients died and in 96 of these an autopsy examination was performed. In 36 patients there was cerebral oedema and the mean age of this group was significantly younger than the other fatal cases. In 28 patients death was attributed to major haemorrhage which originated in the gastrointestinal tract in 25. The prothrombin time ratio was not significantly greater in patients with major bleeding than in those without but they did have a significantly lower platelet count. Sepsis contributed to death in 12 patients. In 25 patients massive hepatic necrosis only was found at autopsy and death was considered to be due solely to hepatic failure. The degree of hepatocyte loss was assessed in 80 fatal cases by a histological morphometric technique on a needle specimen of liver taken immediately post-mortem. The proportion of the liver volume occupied by hepatocytes (hepatocyte volume fraction, HVF) was greatly reduced in all patients (normal 85+/-SD 5 percent) but the mean value was significantly higher in the patients dying with sepsis, cerebral oedema or haemorrhage than in the group in whom death was attributed solely to hepatic failure. There were ten patients in whom liver function was improving at the time of death which was due to cerebral (9) or haemorrhage (1). These observations suggest that many patients presently dying from fulminant hepatic failure may be expected to survive, once more effective therapy is available for the complications of the illness.