Soluble Fas and soluble Fas ligand levels in patients with acute hepatic failure

Nakae, Hajime; Narita, Komei; Endo, Shunsuke

doi:10.1053/jcrc.2001.25470

Cited by 19 publications

(14 citation statements)

References 30 publications

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“…So far, most investigations to delineate the mechanism have been performed in animal models (comprehensively reviewed by Bantel and Schulze-Osthoff, 2012). Clinically, elevated levels of death ligands or receptors, e.g., CD95L, CD95, TRAIL, TNF-α, TNF receptors and Caspases, have been reported in ALF patients induced by different etiologies (Strand et al, 1998; Ryo et al, 2000; Streetz et al, 2000; Tokushige et al, 2000; Nakae et al, 2001; Rivero et al, 2002; Volkmann et al, 2008), suggesting an association between apoptosis and MHN in progression of ALF. On the other hand, necrosis is considered a prominent death pathway of hepatocytes in some drug-induced ALFs.…”

Section: Mechanism Of Mhnmentioning

confidence: 99%

Two sides of one coin: massive hepatic necrosis and progenitor cell-mediated regeneration in acute liver failure

et al. 2015

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Massive hepatic necrosis is a key event underlying acute liver failure, a serious clinical syndrome with high mortality. Massive hepatic necrosis in acute liver failure has unique pathophysiological characteristics including extremely rapid parenchymal cell death and removal. On the other hand, massive necrosis rapidly induces the activation of liver progenitor cells, the so-called “second pathway of liver regeneration.” The final clinical outcome of acute liver failure depends on whether liver progenitor cell-mediated regeneration can efficiently restore parenchymal mass and function within a short time. This review summarizes the current knowledge regarding massive hepatic necrosis and liver progenitor cell-mediated regeneration in patients with acute liver failure, the two sides of one coin.

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Section: Mechanism Of Mhnmentioning

confidence: 99%

Two sides of one coin: massive hepatic necrosis and progenitor cell-mediated regeneration in acute liver failure

et al. 2015

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“…Recent data show that the CD95 system is involved in human ALF caused not only by viral hepatitis but also by Wilson’s disease (Strand et al, 1998; Rivero et al, 2002). Increased levels of death ligands or receptors such as CD95L, TNF-α, or TNF receptors (TNF-R) were found in blood of patients with ALF (Ryo et al, 2000; Streetz et al, 2000; Tokushige et al, 2000; Nakae et al, 2001; Volkmann et al, 2008). Particularly, high serum levels of soluble death receptor CD95 have also been found in drug-induced ALF (Tagami et al, 2003; Rutherford et al, 2007).…”

Section: Death Receptor Signaling In Acute Liver Failurementioning

confidence: 99%

Mechanisms of Cell Death in Acute Liver Failure

Bantel¹,

Schulze‐Osthoff²

2012

Front. Physio.

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Acute liver failure (ALF) can be the consequence of various etiologies, that might vary between different geographic regions. Most frequent are intoxications with acetaminophen, viral hepatitis, or liver damage of unknown origin. ALF occurs when the extent of hepatocyte death exceeds the regenerative capacity of the liver. The mode of liver cell death that is predominantly induced in ALF, i.e., apoptosis or necrosis, is still controversial and presumably determined by the etiology, duration, and magnitude of liver injury. Severe liver damage involves oxidative stress and depletion of ATP resulting in necrosis. In contrast, maintenance of ATP stores is required for the execution of apoptosis. Recent data suggest that necrosis resulting from severe liver damage is associated with poor outcome of ALF patients. Discrimination between apoptosis and necrosis might be therefore useful for the identification of ALF patients requiring liver transplantation. Identification of the molecular cell death mechanisms remains an important issue not only for early prediction of ALF outcome, but also for therapeutic interventions. In view of the pleiotropic functions of critical mediators of cell death and tissue regeneration, a particular challenge will be to reduce hepatocellular death without inhibiting the regenerative capacity of the liver. Here, we review the molecular mechanisms of hepatocyte injury and the pathways leading to apoptosis and necrosis, which might represent potential diagnostic and therapeutic targets in ALF.

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“…Experimental studies have also suggested that apoptosis via the soluble Fas (sFas)/Fas-ligand (FasL) signalling system may play an important role in the development of liver failure [19] . High levels of sFas have also been described in certain chronic liver diseases [20,21] .…”

Section: Introductionmentioning

confidence: 99%

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Elsing¹

2007

WJG

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AIM:To evaluate plasma levels of nitrite/nitrate (NOx), soluble Fas (sFas) antigen, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in patients with compensated and acute decompensated cirrhosis and to evaluate mediators causing acute decompensation in liver cirrhosis. METHODS:This prospective study was conducted in the medical intensive care unit of an academic tertiary center. Fifty-five patients with acute decompensation (gastrointestinal hemorrhage, encephalopathy, hydropic decompensation) and twenty-five patients with compensated liver cirrhosis were included. Blood samples were taken for analyses of sFas, Nox, IL-6, TNF-α. Liver enzymes and kidney functions were also tested. RESULTS:In patients with acute decompensation, plasma sFas levels were higher than in non-decompensated patients (15 305 ± 4646 vs 12 458 ± 4322 pg/mL, P < 0.05). This was also true for the subgroup of patients with alcoholic liver cirrhosis (P < 0.05). The other mediators were not different and none of the parameters predicted survival, except for ALT (alanine-aminotransferase). In patients with portal-hypertension-induced acute hemorrhage, NOx levels were significantly lower than in patients with other forms of decompensation (70.8 ± 48.3 vs 112.9 ± 74.9 pg/mL, P < 0.05). When NOx levels were normalized to creatinine levels, the difference disappeared. IL-6, TNF-α and sFas were not different between bleeders and non-bleeders. In decompensated patients sFas, IL-6 and NOx levels correlated positively with creatinine levels, while IL-6 levels were dependent on Child class. CONCLUSION:In acute decompensated cirrhotic patients sFas is increased, suggesting a role of apoptosis in this process and patients with acute bleeding have lower NOx levels. However, in this acute complex clinical situation, kidney function seems to have a predominant influence on mediator levels.

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Soluble Fas and soluble Fas ligand levels in patients with acute hepatic failure

Cited by 19 publications

References 30 publications

Two sides of one coin: massive hepatic necrosis and progenitor cell-mediated regeneration in acute liver failure

Two sides of one coin: massive hepatic necrosis and progenitor cell-mediated regeneration in acute liver failure

Mechanisms of Cell Death in Acute Liver Failure

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

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