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Acute Liver Failure Caused by Amanita phalloides Poisoning  [PDF]
Luca Santi,Caterina Maggioli,Marianna Mastroroberto,Manuel Tufoni,Lucia Napoli,Paolo Caraceni
International Journal of Hepatology , 2012, DOI: 10.1155/2012/487480
Abstract: Mushroom poisoning is a relatively rare cause of acute liver failure (ALF). The present paper analyzes the pathogenesis, clinical features, prognostic indicators, and therapeutic strategies of ALF secondary to ingestion of Amanita phalloides, which represents the most common and deadly cause of mushroom poisoning. Liver damage from Amanita phalloides is related to the amanitins, powerful toxins that inhibit RNA polymerase II resulting in a deficient protein synthesis and cell necrosis. After an asymptomatic lag phase, the clinical picture is characterized by gastrointestinal symptoms, followed by the liver and kidney involvement. Amatoxin poisoning may progress into ALF and eventually death if liver transplantation is not performed. The mortality rate after Amanita phalloides poisoning ranges from 10 to 20%. The management of amatoxin poisoning consists of preliminary medical care, supportive measures, detoxification therapies, and orthotopic liver transplantation. The clinical efficacy of any modality of treatment is difficult to demonstrate since randomized, controlled clinical trials have not been reported. The use of extracorporeal liver assist devices as well as auxiliary liver transplantation may represent additional therapeutic options. 1. Introduction Acute liver failure (ALF) can be caused by the ingestion of mushrooms containing exceptionally powerful hepatotoxins [1]. Among mushroom intoxications, the amatoxin syndrome is of primary importance because it accounts for about 90% of fatalities [2]. It is characterized by an asymptomatic incubation period followed by the gastrointestinal and hepatotoxic phases, leading eventually to multiorgan failure and death. Although the exact incidence of mushroom poisoning is not precisely estimated due to a presumably relatively high number of underreporting cases, amatoxin poisoning is a worldwide problem. Approximately 50–100 fatal cases are reported every year in Western Europe, being less common in the United States; however, cases of amatoxin poisoning from Africa, Asia, Australia, and Central and South America have been also described [1, 2]. Amatoxin poisoning is caused by mushroom species belonging to three genera Amanita, Galerina, and Lepiota, with the majority of the fatalities attributable to Amanita phalloides, commonly known as the death cap [3] (Figure 1). Figure 1: Image of the mushroom Amanita phalloides, commonly known as the death cap. Being the most common and deadly cause of mushroom poisoning, the present paper analyzes the pathogenesis, clinical features, prognostic indicators, and
Primary hepatic lymphoma presenting as fulminant hepatic failure with hyperferritinemia: A case report
Fyeza S Haider, Robert Smith, Sharif Khan
Journal of Medical Case Reports , 2008, DOI: 10.1186/1752-1947-2-279
Abstract: We present the case of a middle-aged woman exhibiting pancytopenia, hyperferritinemia and rapidly deteriorating to develop acute hepatic failure. Her initial clinical picture led to a working diagnosis of adult onset Still's disease with probable hemophagocytic syndrome before her worsening liver function necessitated a percutaneous liver biopsy and establishment of the final diagnosis of primary hepatic lymphoma.Primary hepatic lymphoma is an uncommon malignancy and its manifestation as progressive hepatitis or acute fulminant hepatic failure can be difficult to diagnose. The presence of constitutional symptoms, pancytopenia and high ferritin levels can complicate the evaluation process. A liver biopsy early in the course of liver dysfunction may establish the diagnosis without a higher risk of bleeding complications seen once liver failure sets in.Primary Hepatic Lymphoma (PHL) is a rare variant of non-Hodgkin's lymphoma with an incidence of < 1%. The presence of diffuse hepatic involvement is uncommon and therefore presentation as hepatocellular jaundice or acute fulminant hepatic failure is rare.We present a case where persistent fever, non-specific symptoms, pancytopenia and strikingly high levels of serum ferritin preceded the presentation of acute liver failure. Due to these findings, alternative diagnoses were entertained including hemophagocytic syndrome in association with adult onset Still's disease (AOSD).A 53-year-old Caucasian woman was transferred to our facility for 3 weeks of intermittent fevers, chills, weight loss, myalgias and arthralgias. She had mild epigastric discomfort with nausea and vomiting. Dalteparin and warfarin were started for a recently diagnosed pulmonary embolism. Her past history was remarkable for diabetes mellitus type 2, hypertension and villous adenoma of the colon. Subsequent colonoscopies were normal. Except for mild epigastric tenderness, her physical examination findings were normal. White blood cell (WBC) count was 4.5 K
Acute Liver Failure Caused by Amanita phalloides Poisoning  [PDF]
Luca Santi,Caterina Maggioli,Marianna Mastroroberto,Manuel Tufoni,Lucia Napoli,Paolo Caraceni
International Journal of Hepatology , 2012, DOI: 10.1155/2012/487480
Abstract: Mushroom poisoning is a relatively rare cause of acute liver failure (ALF). The present paper analyzes the pathogenesis, clinical features, prognostic indicators, and therapeutic strategies of ALF secondary to ingestion of Amanita phalloides, which represents the most common and deadly cause of mushroom poisoning. Liver damage from Amanita phalloides is related to the amanitins, powerful toxins that inhibit RNA polymerase II resulting in a deficient protein synthesis and cell necrosis. After an asymptomatic lag phase, the clinical picture is characterized by gastrointestinal symptoms, followed by the liver and kidney involvement. Amatoxin poisoning may progress into ALF and eventually death if liver transplantation is not performed. The mortality rate after Amanita phalloides poisoning ranges from 10 to 20%. The management of amatoxin poisoning consists of preliminary medical care, supportive measures, detoxification therapies, and orthotopic liver transplantation. The clinical efficacy of any modality of treatment is difficult to demonstrate since randomized, controlled clinical trials have not been reported. The use of extracorporeal liver assist devices as well as auxiliary liver transplantation may represent additional therapeutic options.
Hyperferritinemia Is Associated with Insulin Resistance and Fatty Liver in Patients without Iron Overload  [PDF]
Robert Brudevold, Torstein Hole, Jens Hammerstr?m
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003547
Abstract: Objective During the last 10 years we have experienced an increasing number of referrals due to hyperferritinemia. This is probably due to increased awareness of hereditary hemochromatosis, and the availability of a genetic test for this condition. Most of these referred patients were over-weight middle-aged men with elevated ferritin levels, but without the hemochromatosis-predisposing gene mutations. We evaluated the relationship between hyperferritinemia and the metabolic syndrome in 40 patients. Methods Forty consecutive patients referred for hyperferritinemia were investigated. The examination programme included medical history, clinical investigation and venous blood samples drawn after an overnight fast. This resulted in 34 patients with unexplained hyperferritinemia, which were further examined. Liver biopsy was successfully performed in 29 subjects. Liver iron stores were assessed morphologically, and by quantitative phlebotomy in 16 patients. Results The majority of the patients had markers of the metabolic syndrome, and 18 patients (52%) fulfilled the IDF-criteria for the metabolic syndrome. Mean body mass index was elevated (28,8±4,2), mean diastolic blood pressure was 88,5±10,5 mmHg, and mean fasting insulin C-peptide 1498±539 pmol/l. Liver histology showed steatosis and nuclear glycogen inclusions in most patients (19 out of 29). Only four patients had increased iron stores by histology, of which two could be explained by alcohol consumption. Fourteen of 16 patients normalized ferritin levels after phlebotomy of a cumulative blood amount corresponding to normal iron stores. Ferritin levels were significantly related to insulin C-peptide level (p<0.002) and age (p<0.002). Conclusion The present results suggest that liver steatosis and insulin resistance but not increased iron load is frequently seen in patients referred for suspected hemochromatosis on the basis of hyperferritinemia. The ferritin level seems to be positively associated to insulin resistance.
Failure of titer of contact hypersensitivity to correlate with clinical severity and therapeutic response in contact dermatitis caused by parthenium  [cached]
Verma Kaushal,Manchanda Yashpal,Dwivedi S
Indian Journal of Dermatology, Venereology and Leprology , 2004,
Abstract: Background: The titer of contact hypersensitivity (TCH) has been used to determine the degree of contact hypersensitivity in patients with contact dermatitis. The values have been found to vary in different individuals and also in the same individual at different times apparently due to the varying severity of the disease. We evaluated the correlation of TCH with disease severity and therapeutic response in patients of contact dermatitis caused by the plant Parthenium hysterophorus. Methods: Forty-two patients, 30 (71.4%) males and 12 (28.6%) females, aged between 30-75 years, having air-borne contact dermatitis to Parthenium hysterophorus for 0.5-20 years were included in the study. The disease severity and TCH at baseline were recorded in all the patients. They were treated with azathioprine and followed up every month for 4-69 months. The TCH was repeated every 3 months and the last recorded TCH value was taken for analysis in each patient. Results: The baseline clinical severity score (CSS) varied from 10-80 (mean ± SD: 35.47 ± 19.41) in these patients. It ranged from 10-30 in 22 (52.4%) patients, from 31-50 in 14 (33.3%) patients, and was more than 50 in 6 (14.3%) patients. The baseline TCH to Parthenium was undiluted (UD) in 2 (4.8%), 1:10 in 15 (35.7%), 1:100 in 20 (47.6%), and 1:1000 in 5 (11.9%) patients respectively. At the end of the study, the clinical severity of the disease decreased in most of the patients. The CSS came down to 0 in 31 patients, to 10-20, and to 50 in 4 patients each, but remained stable in three patients who had baseline CSS from 20-40. The overall mean CSS came down from 35.47 ± 19.41 to 4.76 ± 9.43 (p = 0.002). However, there was no significant change in the TCH levels over time (p = 0.153). The last TCH value was negative in 2 (4.8%) patients, undiluted in 5 (11.9%), 1:10 in 10 (23.8%), 1:100 in 18 (42.9%), and 1:1000 in 7 (16.7%) patients. There was no change in the TCH values in 16 (38.1%) patients while it increased or decreased by 1-2 dilutions in 12 (28.6%) patients each. Conclusions: We therefore conclude that the TCH does not correlate with the clinical severity of contact dermatitis or response to treatment.
Dapsone syndrome with acute renal failure during leprosy treatment: case report
Alves-Rodrigues, Edson Nogueira;Ribeiro, Luciano Correa;Silva, Margareth Dióz;Takiuchi, Arley;Fontes, Cor Jesus Fernandes;
Brazilian Journal of Infectious Diseases , 2005, DOI: 10.1590/S1413-86702005000100014
Abstract: dapsone syndrome is a rare hypersensitivity reaction to dapsone and is characterized by high fever, papular or exfoliative dermatitis, progressing to liver toxicity and generalized lymphadenopathy, resembling a mononucleosis infection. we report a patient who developed acute renal failure, as well as other complications characteristic of dapsone syndrome, during leprosy treatment. renal involvement had not been previously described as a dapsone syndrome feature.
Sorafenib-Induced Liver Failure: A Case Report and Review of the Literature
Anneleen Van Hootegem,Chris Verslype,Werner Van Steenbergen
Case Reports in Hepatology , 2011, DOI: 10.1155/2011/941395
Abstract: In patients with hepatocellular carcinoma characterized by vascular invasion and/or extrahepatic disease, Sorafenib is considered treatment of choice. Although mild liver test abnormalities were reported in less than 1% of the patients in the two large randomized, controlled phase III trials, four cases of severe acute Sorafenib-induced hepatitis have been described. One of these four cases died from liver failure. In this paper, a patient with HCC with lung metastases developed high fever and a severe hepatitis that rapidly evolved into liver coma and death, two weeks after the initiation of Sorafenib. Biochemical parameters pointed to a hepatocellular type of injury. Clinical and biochemical presentations were compatible with a drug-induced hypersensitivity syndrome such as it has mainly been described for aromatic anticonvulsants, sulphonamides, and allopurinol. We hypothesize that an underlying cytochrome P450 dysfunction with the presence of reactive drug metabolites might lead to this potentially fatal Sorafenib-induced severe liver dysfunction.
Severe drug hypersensitivity syndrome due to sulphasalazine in patient with rheumatoid arthritis  [cached]
M. Gutierrez,E. Filippucci,L. Bugatti,C. Bertolazzi
Reumatismo , 2011, DOI: 10.4081/reumatismo.2009.65
Abstract: Drug Hypersensitivity Syndrome, also known as Drug Rash with Eosinophilia and Systemic Symptoms is a severe adverse reaction characterized by clinical manifestations including fever, skin eruption, lymphoadenopathy, associated with eosinophilia, leukocytosis and multiple visceral involvement, with 10% of mortality due to development of multiple organ failure. This reaction usually occurs between two and six-eight weeks after the beginning of the treatment and may not resolve with interruption of the suspected drug. Sulfonamides, anticonvulsant, allopurinol are the most frequently involved molecules, but recently cases have been described also with gabapentin and strontium ranelate. In the present report we describe a case of a patient with rheumatoid arthritis who presented severe drug hypersensitivity syndrome, with liver and kidney involvement due to sulphasalazine.
Fulminant Hepatic Failure Caused by Diffuse Liver Metastases Following Gastrointestinal Stromal Tumor Resection
Abdel-Rauf Zeina, Alicia Nachtigal, Eugene Vlodavsky and Jochanan E. Naschitz
Clinical Medicine Insights: Gastroenterology , 2012,
Abstract: Metastatic tumors to the liver resulting in fulminant hepatic failure are a rare occurrence and have not been previously described in patients with gastrointestinal stromal tumor (GIST). A 70 year-old man was referred to hospital with postprandial discomfort. On examination a 19.5 cm large epithelioid GIST of the stomach was diagnosed. The mass exhibited unfavorable prognostic features: mitotic index 18/50 high-power fields, large primary tumor size and male sex. Complete tumor resection with negative margins was achieved and metastases were not detected. The patient presented six months later with jaundice, asterixis and elevated liver enzymes. Computerized tomography showed multiple liver hypodense lesions representing metastases. Treatment with imatinib mesylate was of no avail and the patient died 3 days later as the result of hepatic failure. Massive liver metastases can, even though rarely, be responsible for fulminant hepatic failure. Clinical and radiological follow-up are crucial in patients with GIST even after surgical resection.
Acute liver failure caused by concurrent autoimmune hepatitis and hepatitis B in a 16-year old girl  [cached]
Ma?gorzata Paw?owska, Waldemar Halota
World Journal of Hepatology , 2010,
Abstract: A 16 year-old girl was admitted to hospital because of fatigue and somnolence, nausea, epistaxis and jaundice. Physical examination revealed jaundice, an enlarged liver and tenderness of upper right abdomen. Laboratory tests revealed an increased level of acute liver failure, bilirubin, bile acids, GGTP and a decreased prothrombin ratio, with elevated gamma-globulin and IgG levels, and the presence of anti-mitochondrial M2 antibodies and HBV infection markers. The patient was diagnosed with liver failure resulting from chronic hepatitis B with an autoimmune component. The treatment consisted of steroids, azathioprine, vitamin K, low-protein diet and lactulose enemas. After undergoing a molecular test (HBV DNA 3.23 × 105 IU/mL and mutations I 204 and I 80), the treatment was modified by adding entecavir. After one month the patient was discharged in good clinical condition, with the recommendation of continued entecavir, prednisone and azathioprine. In subsequent months, no clinical deterioration or abnormal biochemical liver function test results were found, despite the discontinuation of immunosuppressive therapy after 10 mo. The patient continues entecavir therapy.
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