Disease relevance of Massive Hepatic Necrosis

• Fatal massive hepatic necrosis: a probable hypersensitivity reaction to sulfasalazine [1].
• Eleven rats in experimental hepatic coma following acute massive hepatic necrosis had blood levels four to 18 times the average normal, and seven cirrhotic patients with hepatic encephalopathy or coma had blood levels four to five times the average normal [2].
• Serum alpha-fetoprotein (AFP) may be detected in patients with nonneoplastic liver diseases such as massive hepatic necrosis, viral hepatitis, and experimental liver injury, AFP levels have not been serially assessed in patients with alcoholic liver disease, with or without cirrhosis, during the period following cessation of alcohol [3].

High impact information on Massive Hepatic Necrosis

• Massive hepatic necrosis in a patient receiving allopurinol [4].
• Fatal massive hepatic necrosis following acetaminophen overdose [5].
• An injection of lipopolysaccharide resulted in massive hepatic necrosis and high mortality in the mice within 24 hours [6].
• These findings indicate that the rise in serum AFP in massive hepatic necrosis is related to the duration of survival after the onset of illness, but does not necessarily imply ultimate recovery [7].
• Histological sections of the hepatocyte growth factor-treated BNL CL.2 cell colonies resembled neocholangioles, believed to include facultative stem cells, which proliferate after submassive and massive hepatic necrosis [8].

Chemical compound and disease context of Massive Hepatic Necrosis

• Intravenous injection of lipopolysaccharide and D-galactosamine, at doses of 0.2 micrograms/kg and 800 mg/kg, respectively, elicited massive hepatic necrosis within 24 hr in C3H/HeN mice [9].
• Protective effects of FUT-175 on acute massive hepatic necrosis induced in mice following endotoxin injection and immunization with liver proteins [10].
• Massive hepatic necrosis in a child after administration of phenobarbital [11].
• CONCLUSION: Our findings suggested that monitoring the soluble TNF receptor-I level may help to assess the prognosis of acute-type fulminant hepatitis and that TNF might be associated with massive hepatic necrosis [12].
• Massive hepatic necrosis associated with accidental imidocarb dipropionate toxicosis in a dog [13].

Biological context of Massive Hepatic Necrosis

• We hypothesized that the HepPar1+ CK19+ progenitor cells are activated during human liver regeneration after massive hepatic necrosis and proliferate with the formation of so-called ductular hepatocytes or neocholangioles [14].

Anatomical context of Massive Hepatic Necrosis

• Use of prostaglandin I2 analog in treatment of massive hepatic necrosis associated with endothelial cell injury and diffuse sinusoidal fibrin deposition [15].

Gene context of Massive Hepatic Necrosis

• BACKGROUND/AIMS: In massive hepatic necrosis, hepatic stem cells constitute a canal of Hering derived, cytokeratin 19 (CK19) positive 'ductular reaction' (DR) [16].
• CK14, CK19, vimentin, and HepPar1 antigen were localized by immunoperoxidase staining in 13 human livers with regeneration after massive hepatic necrosis [14].
• While untreated mice infected with CB1 died within 5 days because of massive hepatic necrosis, the liver was spared in mice immunized with CB3W-RD and then challenged with CB1 [17].
• To investigate the role of TNF-alpha in the mechanism of massive hepatic necrosis, we studied a mouse model of TNF-alpha and D-galactosamine (GalN) -induced hepatic necrosis by ultrastructural analysis [18].
• The co-administration of GalN (700 mg kg(-1), i.p.) and LPS (5 microg kg(-1), i.p.) greatly elevated serum concentrations of tumour necrosis factor-alpha (TNF-alpha), alanine aminotransferase and aspartate aminotransferase, and induced massive hepatic necrosis and lethality in 100% of control mice [19].

References