Cause Of Fulminant Hepatic Failure Research Articles

Fulminant hepatic failure: Summary of a workshop

Fulminant hepatic failure (FHF) is defined by the appearance of severe liver injury with hepatic encephalopathy in a previously healthy person. There are an estimated 2,000 cases of FHF in the United States yearly, representing 0.1% of all deaths and, perhaps, 6% of liver-related deaths. The causes of FHF are many, the chief ones in the United States being hepatitis A; B; non-A, non-B and drug induced liver disease. There are no specific therapies for FHF, however, liver transplantation is recommended for situations in which spontaneous recovery appears unlikely. Factors that are valuable in assessing the likelihood of spontaneous recovery are static features such as patient age and etiology of FHF and dynamic features including encephalopathy grade, prothrombin time, and serum bilirubin. Presently, approximately 7% of all liver transplants are done for FHF and the 1-year patient survival rates average 63%, somewhat less than survival rates for nonfulminant liver disease, averaging 78%. The management of patients with FHF is challenging, particularly important being monitoring and early treatment of infections, hemodynamic abnormalities, and brain edema. Innovative approaches to management and therapy include use of cytoprotective or antiviral medications, hepatic support systems, extracorporeal liver support, hepatocyte transplantation, auxiliary liver transplantation, and xenotransplantation. None of these are of proven benefit, but many are promising as a means to support the patient with FHF until spontaneous recovery occurs or a suitable liver graft is available for transplantation.

Fulminant hepatic failure: Summary of a workshop

Fulminant hepatic failure (FHF) is defined by the appearance of severe liver injury with hepatic encephalopathy in a previously healthy person. There are an estimated 2,000 cases of FHF in the United States yearly, representing 0.1% of all deaths and, perhaps, 6% of liver-related deaths. The causes of FHF are many, the chief ones in the United States being hepatitis A; B; non-A, non-B and drug induced liver disease. There are no specific therapies for FHF, however, liver transplantation is recommended for situations in which spontaneous recovery appears unlikely. Factors that are valuable in assessing the likelihood of spontaneous recovery are static features such as patient age and etiology of FHF and dynamic features including encephalopathy grade, prothrombin time, and serum bilirubin. Presently, approximately 7% of all liver transplants are done for FHF and the 1-year patient survival rates average 63%, somewhat less than survival rates for nonfulminant liver disease, averaging 78%. The management of patients with FHF is challenging, particularly important being monitoring and early treatment of infections, hemodynamic abnormalities, and brain edema. Innovative approaches to management and therapy include use of cytoprotective or antiviral medications, hepatic support systems, extracorporeal liver support, hepatocyte transplantation, auxiliary liver transplantation, and xenotransplantation. None of these are of proven benefit, but many are promising as a means to support the patient with FHF until spontaneous recovery occurs or a suitable liver graft is available for transplantation.

THE CURRENT MANAGEMENT OF PARACETAMOL OVERDOSAGE

SUMMARY Paracetamol overdosage is a common problem, but severe poisoning occurs in only a small percentage of cases. A patient who has suffered paracetamol overdosage should be monitored carefully to ensure that a specialist liver unit can be contacted at the earliest signs of severe poisoning for optimal management and transfer. Paracetamol overdosage remains the most common cause of fulminant hepatic failure in the UK, with a mortality rate of 90%, but survival rates can be improved dramatically by specialist intensive care management, and with the advent of transplantation a previously untreatable group of patients can be treated successfully. However, a patient who is inadequately monitored and treated in the early stages after an overdose may deteriorate to an extent that renders them unsalvable by the time they arrive at the specialist centre.

Hepatitis C and E in non-A non-B fulminant hepatic failure: a polymerase chain reaction and serological study

A significant proportion of patients with fulminant hepatic failure have clinical, biochemical and histological features suggestive of acute viral hepatitis, without serological evidence of either hepatitis A or B. The contribution of hepatitis C to such cases of non-A non-B fulminant hepatic failure is presently uncertain while hepatitis E is well recognized as a cause of fulminant hepatic failure in endemic areas. Nested polymerase chain reaction for detection of both hepatitis C and E virus as well as two serological assays for anti-hepatitis C virus and anti-hepatitis E virus western blotting (both IgG and IgM) were performed on acute sera of 42 consecutive cases of non A, non B-fulminant hepatic failure and on convalescent sera of 17 of 20 patients who underwent orthotopic liver transplantation. Fresh liver tissue, obtained at the time of transplantation, was also studied by polymerase chain reaction in eight cases. Evidence of an acute hepatitis E virus infection (hepatitis E virus RNA amplified from serum by polymerase chain reaction or serum IgM positive to western blot) was found in eight patients. One patient had anti-HCV at presentation but assays on later sera proved negative. Convalescent sera and sera obtained after orthotopic liver transplantation were all negative to both anti-HCV assay systems, but HCV RNA was not found in either serum or liver tissue in any case.(ABSTRACT TRUNCATED AT 250 WORDS)

Mushroom Poisoning

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.

Hepatitis B virus and apparent fulminant non-A, non-B hepatitis

While there is evidence that hepatitis C virus (HCV) does not cause fulminant non-A, non-B hepatitis, the causal agent remains unknown. To evaluate the role of hepatitis B virus (HBV) in this disease, we used a two-step polymerase chain reaction (PCR) to amplify the surface and core regions of HBV DNA in serum and liver samples taken prospectively from twenty-six patients (mean age 36 years, range 1 to 64) with acute hepatic failure undergoing liver transplantation. HBV DNA was absent from the serum of all patients before transplantation. Seventeen patients were diagnosed as having non-A, non-B hepatitis because they lacked serological evidence of hepatitis A virus or HBV infection. Liver samples were taken from twelve of these patients, and six samples were positive for HBV DNA. By contrast HBV DNA was not detected in liver from three patients with acute liver failure caused by hepatitis A or toxins. HCV RNA was not found in pretransplant samples by PCR. Four of the six patients with detectable HBV DNA in liver and presumptive non-A, non-B hepatitis had detectable HBV DNA in serum after transplantation. One additional patient who did not donate pretransplant liver had HBV DNA in a post-transplant serum sample. Thus, HBV DNA was present before or after transplantation in seven of seventeen patients with apparent non-A, non-B hepatitis. Three of five patients with detectable post-transplant serum HBV DNA were serologically positive for HBV surface antigen. These findings indicate that HBV may be a common cause of fulminant hepatic failure in patients lacking serological evidence of HBV infection.

New Approaches to Paracetamol Hepatotoxicity

Paracetamol overdose leading to hepatotoxicity remains the most common cause of fulminant hepatic failure in England and Wales. Studies at the Institute of Liver Studies have demonstrated that the continuing mortality is, at least in part, due to an increase in the severity of fulminant hepatic failure secondary to chronic alcohol consumption or the long term use of anticonvulsant drugs.

Congestive heart failure as cause of fulminant hepatic failure

In this patient with long-standing cardiomyopathy and congestive heart failure the syndrome of fulminant hepatic failure developed on two occasions; he recovered both times. There was no evidence of viral or toxic hepatitis as a cause of his liver failure. We conclude that in this case, aggravation of long-standing congestive heart failure may have led to severe hepatocellular necrosis with signs of encephalopathy not commonly observed.