Apoptotic Mechanisms in Fulminant Hepatic Failure
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Pathogenesis of fulminant hepatic failure (FHF) in nonacetaminophen etiology is not elucidated. We have investigated the significance of tumor necrosis factor (TNF) type-I receptor (TNF-R1) and Fas receptor (CD95, APO-1) in FHF.Liver biopsy samples were obtained from 14 FHF patients. Liver tissue samples of 10 patients with acute viral hepatitis (AVH) and 10 cases who died, unrelated to liver disease served as tissue biopsy controls. Immunohistochemical methods were employed to analyze expression of TNF-R1 and Fas expression in hepatocytes.Immunohistochemical analysis revealed high expression (P<0.001) of Fas and TNF-R1 in FHF cases in relation to AVH cases. This expression was more in cytoplasm of apoptotic hepatocytes than viable swollen hepatocytes and this correlated with the extent of hepatocyte apoptosis. The mean apoptotic index was significantly (P<0.001) higher in FHF in relation to AVH.Enhanced expression of TNF-R1 and Fas receptors on the apoptotic hepatocytes suggest that both may be involved in the pathogenesis of FHF and seem to be potential therapeutic target.Keywords:
Fulminant hepatic failure
Pathogenesis
Fulminant
Fulminant hepatitis
Fulminant hepatitis
Fulminant
Hepatitis B
Viral Hepatitis
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The article deals with the problem of fulminant viral hepatitis at the present stage. Are given their own observation of children, patients with fulminant hepatitis B. The data, including clinical examples show that fulminant hepatitis B occurs in born to HBV-infected mothers to infants during the first six months of life, which has not been evaluated vaccine prevention of hepatitis B, and is characterized by a high level of mortality.
Fulminant hepatitis
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To explore the dangerous factors of the bad prognosis of fulminant hepatic failure. We analyzed the relation between prognosis and age, etiologic feature, complication, index of laboratory examination. When the patients who were more young, the survival rate were more higher.The serum levels of AST/ALT,TBil/DBil,TBA were significantly higher in the blood samples from the death group than from the survivor group. The level of Tch was contrary. The survival rate was significantly higher in patients whose PTA 40% , and similar result was obtained in patients whose APTT 45 seconds. The age, the complication and the index of the laboratory examination are the important factors in judging the prognosis of fulminant hepatic failure.
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Fulminant hepatic failure
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The possible importance of humoral immunity in the pathogenesis of fulminant hepatitis was investigated by comparing 17 patients with fulminant hepatitis type B with 20 patients with severe but non-fulminant disease. Hepatitis B surface antigen (HBsAg) was cleared from the serum significantly faster (P less than 0-001) in those with fulminant hepatitis, and in 41% anti-HBsAg (HBsAb) was detectable by radioimmunoassay (RIA) at presentation. In all 11 sera from patients with fulminant hepatitis that were examined by electron microscopy aggregates of HBsAg and HBsAb were seen. In contrast, HBsAb was never detected by RIA in those with non-fulminant hepatitis, and in only one serum specimen (5%) were aggregates seen on electron microscopy. A significant sex difference between fulminant and non-fulminant hepatitis was observed, 65% of patients with fulminant hepatitis but only 15% of patients with non-fulminant hepatitis being women (P less than 0-01). An enhanced production of HBsAb in fulminant hepatitis, by leading to free HBsAb in portal blood, may cause an Arthus reaction in the sinusoids of the liver with ensuing ischaemic necrosis of hepatocytes.
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Fulminant hepatitis
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Cerebral oedema is a common cause of death in patients with fulminant hepatic failure (Brajtbord et al, 1989). The relationship between cerebral oedema and fulminant hepatic failure is reviewed. The current diagnosis and treatment of cerebral oedema is discussed. Intracranial pressure monitors allow for early detection and treatment of cerebral oedema. Further research is required to evaluate the efficacy of each method.
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The histological findings of fulminant hepatic failure were correlated to the demographic, clinical, biochemical and virological features in children and adolescents, native to the Amazonas State in Northern Brazil. 96.2% had evidence of infection by primary hepatotrophic viruses. Histological analysis revealed three distinct patterns of fulminant hepatic failure.
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Summary Tumour necrosis factor-alpha (TNF-α), a cytokine derived from macrophages, is considered to bean important endogenous mediator of endotoxic shock. Patients with fulminant hepatic failure are particularly susceptible to infection and the development of multi-organ failure and similarities to endotoxic shock suggest a possible pathogenetic role for TNF in fulminant hepatic failure. In vitro TNF production was therefore investigated serially in 21 consecutive patients with fulminant hepatic failure and in 21 healthy controls. Spontaneous and lipopolysaccharide-stimulated TNF production were elevated in viral-induced fulminant hepatic failure, compared with healthy controls (P < 0.05 and P <0.01, respectively). By contrast, patients with paracetamol-induced fulminant hepatic failure had normal spontaneous and lipopolysaccharide-stimulated TNF production, while those who died had significantly reduced spontaneous TNF production compared with survivors (P < 0.02); this difference was present throughout admission. In this group elevations in TNF production above baseline were associated with Gram-positive bacterial or fungal infection but not Gram-negative bacterial infection. There was no correlation between any of the clinical complications of fulminant hepatic failure and TNF production. These studies indicate that TNF is produced in response to microbial stimuli in fulminant hepatic failure, but do not support a direct role for TNF in the evolution of the clinical complications of fulminant hepatic failure.
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Fulminant
Fulminant hepatic failure
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Viral Hepatitis
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In most cases of drug-induced liver injury, it is difficult to diagnose whether these cases would progress to fulminant hepatic failure. We investigated the characteristics of non-viral and suspiciously drug-induced fulminant hepatic failure by comparing clinical data between cases that progressed and those that did not progress to fulminant hepatic failure.Ninety-five cases of suspicious drug-induced liver injury including 22 cases that had been treated at our hospital, and subsequently progressed to fulminant hepatic failure were involved in this study. We investigated the characteristics of drug-induced fulminant hepatic failure by a comparison of non-fulminant and fulminant cases, and simultaneously of survivors and fatal cases in the group of fulminant cases.Many of the clinical variables were significantly deteriorated in fulminant cases. The latent period, which means the duration of drug administration, correlated with the severity of drug-induced liver injury including fulminant hepatic failure. Suspicious cases of drug-induced liver injury where the bilirubin level at the time of definite diagnosis stayed over 13 mg/dL for more than one month were likely to progress to fulminant hepatic failure.Our results suggest that the latent period and the peak level of total bilirubin would be prognostic factors for the severity of drug-induced fulminant hepatic failure. Early preparation of liver transplantation should be recommended by referring these characteristics.
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