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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute liver failure (ALF) is a rare but often fatal disorder in childhood. Its aetiology includes infections, toxins, metabolic disorders, infiltrative diseases, autoimmune hepatitis, ischaemia, irradiation damage, but in a high proportion of cases it remains unknown. In contrast to adults, in children with ALF hepatic encephalopathy can be a late event, and may not develop at all, despite a lethal outcome, particularly in infants. Children with ALF should be managed in experienced centres with facilities for liver transplantation. Transplantation should be offered only if the underlying disease is treatable by liver replacement and if the prognosis of transplant is better than that of the underlying disease, as in many cases of ALF the liver has the potential to recover with supportive treatment, if the child is kept alive and stable long enough. Universally accepted criteria for listing for transplantation have not been defined as yet. In our centre, maximum INR, bilirubin level, and white cell count, together with age have proven to be reliable predictors of outcome. Future efforts in the management of ALF should concentrate on designing efficient supportive therapy and specific treatments to provide effective non-transplant therapeutic options.
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PMID:Approaches to acute liver failure in children. 1559 30

Acute liver failure is a clinical condition associated with high mortality despite recent technological advances. Supportive devices such as the Molecular Adsorbents Recirculating System (MARS) provide therapeutic strategies to add time to find an organ for orthotopic liver transplantation or to allow the native liver to recover sufficiently to make transplantation unnecessary. In this series of cases, we discuss our initial experiences with three patients with acute liver failure. One patient had high bilirubin levels caused by Epstein-Barr virus infection and responded well after three MARS sessions. In a second patient, MARS therapy was used to treat acute-on-chronic liver failure caused by chronic hepatitis B virus infection that had not been treated previously; because of severe hemodynamic compromise, only one MARS session was performed. The third patient had an initial diagnosis of acute liver failure and cryptogenic hepatitis, and was treated with five MARS sessions as a supportive measure until the definitive diagnosis (metastatic disease) was performed. In all patients, MARS therapy was well tolerated and induced only mild hypokalemia. In conclusion, although MARS therapy was an effective strategy for these cases of liver failure and greatly improved the biochemical variables, its impact on the mortality rate has not yet been determined.
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PMID:Acute liver failure and the Molecular Adsorbents Recirculating System: early experience in a tertiary care hospital in Mexico City. 1565 60

Fulminant hepatic failure (FHF) accounts for 10-15% of pediatric liver transplants in the USA annually. Because the onset of FHF may be the first presentation of Wilson's disease (WD) and autoimmune hepatitis (AIH) in previously asymptomatic adolescents, determination of the etiology of FHF is critical as treatment and prognosis differ between these two entities. Patients with AIH may be salvaged by medical treatment. On the contrary, liver transplantation is currently the only life saving therapeutic option available for patients with WD who present with fulminant liver failure. To establish the diagnosis of WD and AIH in the setting of FHF remains challenging for diagnosticians and decisions regarding liver transplantation may be necessary before a diagnosis is firmly established. We report a previously asymptomatic patient who presented with FHF and clinical and laboratory features suggestive of both WD and AIH and who underwent successful therapeutic liver transplantation before the diagnosis of WD could be confirmed.
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PMID:Fulminant hepatic failure: Wilson's disease or autoimmune hepatitis? Implications for transplantation. 1566 23

Fulminant hepatic failure, which is represented by fulminant hepatitis, is fatal in most cases unless prompt liver transplantation is performed. Even if liver transplantation is performed, irreversible neurological damage is often complicated. In this case report, we describe two cases of fulminant hepatitis induced by acute hepatitis B virus infection, both of which were successfully rescued by living related liver transplantation without significant complications. The case 1 was a 45-year-old Japanese male. He complained general malaise and anorexia. His local physician diagnosed him as acute hepatitis B, and referred to our hospital. Due to severe coagulopathy, plasma exchange was performed 3 times. However, his hepatic coma progressed rapidly along with rapid decrease of both his direct/indirect bilirubin (D/T) ratio and serum blood urea nitrogen (BUN) levels. Living related liver transplantation was performed under the diagnosis of acute fulminant hepatitis B. The case 2 was a 34-year-old Japanese male. His complaints were fever and skin rush. He was referred to our hospital under the diagnosis of acute hepatitis B. On the second day after admission, he developed grade II hepatic coma, which deteriorated into grade III in spite of intensive therapy including plasma exchange. He also demonstrated rapid decrease of both D/T ratio and serum BUN level. Living related liver transplantation was performed on the next day. Both cases recovered without any evidence of neurological sequelae. In general, it is extremely difficult to rescue fulminant hepatitis by conservative treatments, particularly in cases with rapid progression. Although emergency liver transplantation may be an only option to rescue in such a case, living related liver transplantation has an advantage in view of urgent organ donation over cadeveric transplantation.
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PMID:Living related liver transplantation for acute fulminant hepatitis B: experience from two possible hyper-acute cases. 1567 78

Acute liver failure is a complex multisystemic illness that evolves quickly after a catastrophic insult to the liver leading to the development of encephalopathy. The underlying aetiology and the pace of progression strongly influence the clinical course. The commonest causes are paracetamol, idiosyncratic drug reactions, hepatitis B, and seronegative hepatitis. The optimal care is multidisciplinary and up to half of the cases receive liver transplants, with survival rates around 75%-90%. Artificial liver support devices remain unproven in efficacy in acute liver failure.
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PMID:Acute liver failure. 1574 89

The latest advances in hepatology were presented in oral and poster presentations. In order to cover the varying subspecialties, the sessions were divided into various sections including 'Acute Liver Failure and Artificial Liver Support', 'Biliary Tract and Immunologic Liver Diseases', 'Cellular and Molecular Biology', 'Clinical and Experimental Hepatobiliary Surgery', 'Hepatotoxicity and Cell Death', 'Transport and Biliary Physiology', 'Viral Hepatitis', 'Evaluation and Treatment of Biliary Disease', 'Necrosis/Apoptosis', 'Portal Hypertension', 'Blood Flow and Vascular Disorders of Cirrhosis', 'Liver Transplantation', 'Fibrogenesis', 'Hepatocellular Carcinoma', 'Metabolism and Genetic Disease', and 'Public Policy, Epidemiology and Decision Analysis'. Drug therapy focused on treatments for viral hepatitis, autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis, and recurrent viral disease following liver transplant. High dose interferon therapy or various combinations of interferon/ribavirin (ICN Pharmaceuticals Inc) therapy seem to offer the best current therapy for chronic HCV. PEGylated interferon (F Hoffmann-La Roche Ltd) offers hope for treatment and histologic improvement in patients with chronic HCV. Following liver transplantation, combination interferon/ribavirin therapy may also find success, but caution with new potent immunosuppressant monoclonal antibodies is advised. For HBV, intramuscular H-BIG (NABI) appears to be effective and less costly than iv H-BIG administration following liver transplantation. Percutaneous radiofrequency ablation may hold promise over conventional ethanol injection therapy for small hepatocellular carcinoma. Autoimmune hepatitis may respond to tacrolimus therapy whereas budesonide therapy did not provide any advantage to prednisone therapy. For primary biliary cirrhosis, eicosapentate and ursodeoxycholic acid may provide benefit to some patients while silymarin from milk thistle did not provide any additional benefit. In primary sclerosing cholangitis, high dose ursodeoxycholic acid may provide benefit. Ursodeoxycholic acid may also provide benefit for mothers with intrahepatic cholestasis of pregnancy by decreasing pruritus, lowering laboratory values and allowing deliveries to occur closer to term.
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PMID:Digestive disease week 2000. American Association for the Study of Liver Diseases. 1605 98

The aim of our study is to report upon the presentation of two patients with life-threatening acute liver failure (ALF) due to amoxicillin and amoxicillin/clavulanate. A 59-year-old, Caucasian male presented with ALF 34 days after receiving amoxicillin/clavulanate. Despite aggressive supportive care, he died on hospital day 10. A 42-year-old, Caucasian female presented with ALF 21 days after receiving amoxicillin. She underwent successful liver transplantation on hospital day 19. In both cases, all competing causes of ALF had been excluded, liver pathology was consistent with drug-induced hepatitis, and cases were deemed "definite/highly probable" using causality assessment. Amongst 14 prior ALF/death cases due to amoxicillin/clavulanate, the mean age (62 years), male predominance (57%), and mean delay from drug cessation to presentation (17 days) is similar to what has been reported in patients with self-limited cholestatic hepatitis. Acute liver failure is a rare manifestation of amoxicillin and amoxicillin/clavulanate hepatotoxicity with no obvious clinical features at presentation portending a poor prognosis. Early transfer of patients with severe drug-induced hepatotoxicity (i.e., encephalopathy or coagulopathy) to a transplant center is recommended due to their poor likelihood of recovery.
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PMID:Acute liver failure due to amoxicillin and amoxicillin/clavulanate. 1618 74

Fulminant hepatic failure of unknown origin is the most common cause of fulminant hepatitis with high incidence of aplastic anaemia. Furthermore, the association of liver failure and aplastic anaemia has an increased mortality rate. In this report we describe a 16-month-old boy who presented with aplastic anaemia preceding a non-A, non-B, non-C fulminant liver failure. He developed severe graft versus host disease (GvHD) after liver transplantation, proven by the presence of donor cells in the peripheral blood and in the skin biopsy. He received conventional therapy (steroids, mycophenolate, anti-IL-2 monoclonal antibodies, anti-thymocyte globulin) without success. In an attempt to obtain T cell depletion and reduce the GvHD, he was treated with Alemtuzumab, a first time use for this indication. Aplastic anaemia was extensively investigated, especially exploring the possibility of primary immunodeficiency and reticular dysgenesis which were excluded based on clinical history. However, another form of primary immunodeficiency could be the cause of the uncontrollable proliferation of the donor lymphocytes derived from the liver transplant. Despite aggressive treatment GvHD progressed and the patient died of multiorgan failure. The majority of authors mention aplastic anaemia as a secondary event post liver transplant, whereas in our view this might be a haematopoietic stem cell disorder preceding fulminant hepatic failure. These patients also need to be evaluated extensively in order to exclude a primary immunodeficiency. The underlying disease will determine the choice of immunosuppressive treatment, especially in case of development of GvHD caused by the transplanted lymphocytes inhabiting the donor liver.
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PMID:Fatal GvHD as a complication of liver transplantation for undetermined fulminant hepatic failure and associated aplastic anemia. 1705 30

A Saudi family with Wilson's disease (hepatolenticular degeneration) is described. The index case presented with anicteric hepatitis and hydrops of the gallbladder. Neurological involvement appeared later. The diagnosis of Wilson's disease was based on the presence of Kayser-Fleischer rings, a low serum ceruloplasmin level, and an elevated urinary copper concentration. Histological examination of the liver biopsy specimen revealed active cirrhosis. Acute hepatic failure developed during D-penicillamine therapy. Continuation of the drug at a lower dose, along with other supporitve measures, was successful in reversing this. After three years of therapy, the index patient's neurological signs disappeared, and liver function and gallbladder size and function returned to normal. Family screening revealed that three other siblings have the disease, and all have been treated with D-penicillamine. The parents are related but are asymptomatic. An unusual feature of the index case was the presence of a distended nonfunctioning gallbladder that reverted to normal with decoppering. Although D-penicillamine treatment possibly precipitated the acute hepatic failure, paradoxically it was also successful in treating it.
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PMID:Wilson's disease in Saudi Arabia: Report of a Saudi Arab family. 1759 Aug 8

In Japan, patients with hepatitis are diagnosed as having fulminant hepatitis and late-onset hepatic failure (LOHF) when grade II or more severe hepatic encephalopathy develops within 8 weeks and between 8 and 24 weeks, respectively, of the disease onset, with a prothrombin time of less than 40% of the standardized value. Fulminant hepatitis patients are classified into the acute and subacute types, in which the encephalopathy occurs within 10 days and later than 11 days, respectively. According to the nation-wide survey by the Intractable Liver Disease Study Group of Japan, liver transplantation was performed in 14% and 26% of the patients with the acute and subacute types, respectively, and in 19% with LOHF between 1998 and 2003. Survival rate of these patients was 77%, which was greater than those of the patients treated without liver transplantation; 54%, 24% and 12% in the acute and subacute types and LOHF, respectively. The indications for liver transplantation in fulminant hepatitis patients are currently determined according to the Guideline of the Acute Liver Failure Study Group of Japan in 1996, which is based on assessment of the prognosis of the patients at the onset of hepatic encephalopathy and reassessed 5 days later. Predictive accuracy of the Guideline, assessed in the patients between 1998 and 2003, were 68% and 78% among the cases with the acute and subacute types, respectively, of fulminant hepatitis. Liver transplantation was considered in most of LOHF patients at 8 or more days before encephalopathy development. Although liver transplantation improved the prognosis of patients with acute liver failure, the Guideline should be modified to improve the accuracy for fulminant hepatitis patients, and the new criteria should be made for LOHF patients.
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PMID:Indication criteria for liver transplantation for acute liver failure in Japan. 1912 53


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