Disease relevance of Liver Failure

• In a group of patients seen at a referral center, chronic post-transfusion hepatitis C was a progressive disease and, in some patients, led to death from either liver failure or hepatocellular carcinoma [1].
• Liver fibrosis is the common response to chronic liver injury, ultimately leading to cirrhosis and its complications, portal hypertension, liver failure, and hepatocellular carcinoma [2].
• The results demonstrate a potentiation of LPS toxicity by GM-CSF in a mortality model as well as in a septic liver failure model in mice [3].
• MCAD deficiency typically presents in the second year of life as hypoketotic hypoglycemia associated with fasting and may progress to liver failure, coma, and death [4].
• To explore the metabolic aspects of chronic liver disease, diurnal changes of arterial ketone body ratio (acetoacetate/3-hydroxybutyrate), reflecting hepatic mitochondrial redox potential, were investigated in normal subjects, patients with chronic liver disease (Child's class A or B), and patients with hepatic failure (Child's class C) [5].

Psychiatry related information on Liver Failure

• It is presumed that, under pathological conditions (hepatic failure, alcoholic intoxication, succinic semialdehyde dehydrogenase defects), the rate of GHB synthesis or degradation in the peripheral organ is modified and induces increased GHB levels which could interfere with the normal brain mechanisms [6].
• Feeding behavior and ambulatory activity in rats with D-galactosamine-induced hepatic failure [7].
• One patient with a chronic alcohol-drinking history (greater than 200 g/day) received N-acetylcysteine at 12 h but died from liver failure [8].

High impact information on Liver Failure

• Homozygous ERCC-1 mutants were runted at birth and died before weaning with liver failure [9].
• In the patients with acetaminophen-induced liver failure, the infusion of acetylcysteine resulted in an increase in mean oxygen delivery from 856 to 975 ml per minute per square meter of body-surface area (P = 0.0036), due to an increase in the cardiac index from 5.6 to 6.7 liters per minute per square meter (P = 0.0021) [10].
• Hepatic failure from valproic acid [11].
• Only IL-15, but not IL-2, completely protected from lethal hepatic failure [12].
• Carbon monoxide protects against liver failure through nitric oxide-induced heme oxygenase 1 [13].

Chemical compound and disease context of Liver Failure

• Renal glutamine uptake and subsequent urinary ammonia excretion could be an important alternative pathway of ammonia disposal from the body during liver failure (diminished urea synthesis), but this pathway has received little attention [14].
• Uptake of oleate from albumin solutions by rat liver. Failure to detect catalysis of the dissociation of oleate from albumin by an albumin receptor [15].
• Six months later, she experienced a rapidly progressive hepatic failure manifested by elevation of serum bilirubin level, prolongation of prothrombin time, and mild to modest increase of serum aminotransferase levels [16].
• To study in detail the role of the liver in GABA metabolism, uptake and catabolism of GABA by isolated perfused liver from normal rats and rats with galactosamine- or carbon tetrachloride-induced liver failure were measured [17].
• Our experience shows that fibrosing cholestatic hepatitis and liver failure caused by HBV infection can be successfully treated with lamivudine [18].

Biological context of Liver Failure

• Clinical features of rapidly progressive liver failure, indicated by prolonged prothrombin time (57 seconds) and increased bilirubin (40.4 mg/dL) and ammonia (129 mumol/L) concentrations, were accompanied by an extremely high serum HBV DNA level (2.153 x 10(6) pg/mL) [18].
• CONCLUSIONS: Both TNF as well as IFN-gamma are critical mediators of liver injury in concanavalin A-treated mice, whereas hepatic DNA fragmentation and liver failure in the D-galactosamine models depend only on TNF [19].
• Indeed, ABIN-1 was found to prevent not only NF-kappaB activation, but also apoptosis of cultured hepatocytes in response to TNF, explaining its protective effect against TNF-induced liver failure [20].
• Acetaminophen overdose causes massive hepatic failure via mechanisms involving glutathione depletion, oxidative stress, and mitochondrial dysfunction [21].
• Rectal administration of different Lactobacillus strains with and without arginine in an ALI model significantly modulates the extent of the liver failure and reduces bacterial translocation [22].

Anatomical context of Liver Failure

• Interestingly, we found that, compared with control hepatocytes, p27 knockout hepatocytes proliferate better after transplantation into diseased livers to reverse liver failure [23].
• Cytochrome c was released from mitochondria prior to liver failure in the Fah-/- Hpd-/- double-mutant mice after the administration of HGA [24].
• Cerebrospinal fluid glycine levels were increased two to three times in parallel with increasing brain glycine content in the devascularized rat but were unchanged in thioacetamide-induced liver failure, suggesting distinct pathophysiological mechanisms in these two experimental situations [25].
• Moreover, selective expression of gelsolin in sinusoidal endothelial cells indicates a pivotal role for interactions between sinusoidal endothelial cells and liver parenchymal cells in Fas ligand-mediated liver failure [26].
• One patient died of liver failure 3 weeks after right trisegmentectomy with reconstruction of the left hepatic vein and one patient died at 3 months after resection due to sepsis from a segment of small bowel that perforated into a diaphragmatic hernia [27].

Gene context of Liver Failure

• The apoptotic-inducing capacity of naturally processed sFasL was reduced by >1,000-fold compared with membrane-bound FasL, and injection of high doses of recombinant sFasL in mice did not induce liver failure [28].
• The aim of this study was to investigate whether endogenously formed TNF contributes to liver failure caused by hepatotoxins [29].
• Mutations of the SCO1 gene in mitochondrial cytochrome c oxidase deficiency with neonatal-onset hepatic failure and encephalopathy [30].
• Transferrin saturation above 75% was related to iron overload in GH and to liver failure in alcoholic cirrhosis [31].
• Wilson disease is an autosomal recessive copper transport disorder resulting from defective biliary excretion of copper and subsequent hepatic copper accumulation and liver failure if not treated [32].

Analytical, diagnostic and therapeutic context of Liver Failure

• Troglitazone-induced hepatic failure leading to liver transplantation. A case report [33].
• Before surgery, the bile HGF concentrations were minimal (0.8 +/- 0.1 ng/mL); however, after hepatectomy on postoperative day 1 in patients without posthepatectomy liver failure (20 of 24), they increased severalfold (4.1 +/- 0.4 ng/mL, P < .05) [34].
• The blood concentrations of endotoxin were significantly higher after intravenous injection of endotoxin in the D-galactosamine-induced liver failure group (p < 0.05) and decreased much more slowly (p < 0.05) [35].
• Rats with portacaval anastomosis or with hyperammonemia without liver failure also show impaired learning ability and impaired function of the glutamate-nitric oxide-cyclic guanine monophosphate (glutamate-NO-cGMP) pathway in brain [36].
• In addition, several potential diclofenac adducts were identified in the liver of a patient with diclofenac-induced hepatic failure, but not from a normal human donor liver, by immunoblotting with an adduct-selective rabbit antiserum [37].

References