Search results for "Fulminant hepatic failure"

Remission of severe rheumatoid arthritis following liver transplantation.

1993

We present the case of a 32-year-old male who suffered from severe RA from the age of 21 years. After 9 years of active disease and poor response to therapy the patient developed severe hepatitis induced by the NSAID pirprofen. He went into fulminant hepatic failure necessitating emergency liver transplantation. Liver transplantation was followed by clinical and laboratory remission of his RA and he has remained virtually asymptomatic for more than 3.5 years. The possibility that this favourable clinical course was due to the immunosuppressive effect of the liver transplant rather than the ensuing immunosuppressive therapy is discussed.

Fulminant hepatic failure requiring liver transplantation in 22q13.3 deletion syndrome.

2010

We report on a 4-year-old girl with severe developmental delay, absent speech, and chromosome 22q13.3 deletion (Phelan-McDermid syndrome), karyotype 46,XX.ish del(22)(q13.31qter)(ARSA-,N85A-,SHANK3-). At the age of 3 years, she needed an emergency liver transplantation because of fulminant hepatic failure, most likely caused by hyperacute autoimmune hepatitis triggered by a viral infection. This is the second report of a patient with 22q13.3 deletion and fulminant liver failure. By array-CGH we identified in this patient a 5.675 Mb terminal deletion (22q13.31 --> qter; including approximately 55 genes; from NUP50 to RABL2B) and in the previous patient a 1.535 Mb deletion (22q13.32 --> qter;…

Drugs and Toxins Effects on the Liver

2011

Drug induced hepatotoxicity can be defined as a liver injury caused by drug or herbal medicines leading to liver test abnormalities or to a liver dysfunction with a reasonable exclusion of the other competing aetiologies. The liver has a central function in the metabolism of the xenobiotics, and as a result it may be susceptible to its toxic or idiosyncratic effects. While the overall incidence of drug induced liver injury (DILI) is infrequent (1 in 10.000 to 100.000 persons exposed), the impact is significant in the general population, with broad implications for patients, physicians, pharmaceutical industries and governmental regulatory agencies. DILI is the principle reason for the termi…

The role of apoptosis versus oncotic necrosis in liver injury: Facts or faith?

2006

A tightly controlled balance between cell division and cell death is a basic feature for the development and maintenance of liver homeostasis. Disturbances of this balance contribute to liver diseases: too much cell death can cause liver injury, too little cell death is a prerequisite for the development of hepatocellular carcinoma. Thus, a stringent control of the equilibrium of life and death in the liver is necessary. During the last decade most research activities in hepatology dealing with liver injury focussed on the evaluation of apoptosis pathways. Therefore, our understanding of the mechanisms of apoptosis has made profound progress. Programmed cell death (PCD) in the liver enables…

Liver regeneration induced by a designer human IL‐6/ sIL‐6R fusion protein reverses severe hepatocellular injury

2000

The cytokine IL-6 plays a significant role in liver regeneration in conjunction with additional growth factors (HGF, TNF-α, and TGF-α). Many IL-6 effects depend on a naturally occurring soluble IL-6 receptor (sIL-6R). Here, the chimeric protein hyper-IL-6, constructed from the human IL-6 protein fused to a truncated form of its receptor, was found to have superagonistic IL-6 properties, and as such, enhanced liver cell regeneration. Hyper-IL-6 reversed the state of hepatotoxicity and enhanced the survival rates of rats suffering from fulminant hepatic failure after D-galactosamine administration. The hyper-IL-6 protein has a significant potential for use in the treatment of severe human liv…

Hepassocin as a treatment for fulminant hepatic failure: will it translate from rats to human?

2010

Acute liver failure (ALF) is defined as the abrupt loss of hepatic cellular function in a patient without pre-existing liver disease, with the subsequent development of coagulopathy, jaundice and encephalopathy. It remains one of the most challenging medical emergencies, due to the multiorgan nature of the disease, the rapid evolution of the clinical condition and the need for multidisciplinary supportive interventions in order to assess the necessity for liver transplantation (LT) correctly.1 Despite different causes of ALF, the mode of cell death typically follows one of two patterns: necrosis or apoptosis; apoptosis is manifest by nuclear and cytoplasmic shrinkage without disturbance of …

New Therapeutic Aspects in Fulminant Hepatic Failure

1991

D-penicillamine in Wilson's disease presenting as acute liver failure with hemolysis.

1982

Wilson's disease in a young woman presenting with an acute course is described. The clinical manifestations were fulminant hepatic failure associated with marked intravascular hemolysis. Immediate D-penicillamine and high-dose steroid therapy did not influence the course of the disease. Necropsy revealed an increased hepatic copper content and cirrhosis with extensive necrosis of the liver.

The Italian experience on paediatric liver transplantation: 1988-1999 report

2002

Abstract Background. Liver transplantation is the treatment of choice for end-stage liver disease in both adult and paediatric patients. The Italian experience in paediatric liver transplantation during the period 1988–1999 is reported herein. Patients and methods. This report concerns 228 liver transplantations performed in 207 patients (100 male, 107 female, mean age 5.1±4.4 years) in 11 Italian centres. The mean waiting time on the transplantation list was 6. 1±8.9 months and the main indications for the procedure were biliary atresia, inborn metabolic disorders, liver cirrhosis, liver neoplasms, Alagille syndrome, and fulminant hepatic failure. Results. The cumulative survival rate was …