title: [Fulminant or sub-fulminant hepatocellular failure caused by metastatic invasiveness of the liver: an other cause of hypoxic hepatitis?].
abstract: OBJECTIVE
  The purpose of this retrospective study was to report a series of 9 new cases of fulminant hepatic failure due to metastatic liver disease and to identify signs to support a theory of hypoxia.
  
  
  METHODS
  In these 9 cases and in 38 previously published cases of fulminant or subfulminant liver failure, we looked for clinical (shock, sepsis, and cutaneous signs of circulatory failure), laboratory (marked increase in serum aminotransferases levels) and histological (cell necrosis) parameters compatible with liver hypoxia.
  
  
  RESULTS
  Cutaneous signs of circulatory failure or shock were observed in 3 of the 9 cases in this study, and were not due to cardiogenic or septic shock. A marked increase in serum aminotransferases levels, 10 times above the upper limit of normal, was observed in 8 of the 9 cases in the present study and in 23 of 37 cases of the literature. Liver cell necrosis was observed in 6 of the 7 autopsied patients in this series and in 20 of 34 cases in the literature. Generally, liver cell necrosis was more severe than tumor cell necrosis and was related to the degree of sinusoidal involvement by tumoral cells. In one case, hepatic blood flow was decreased despite a high level of cardiac blood flow suggesting impairment of circulation in the liver.
  
  
  CONCLUSIONS
  These 9 cases and a review of the literature support the hypothesis of hypoxic liver cell necrosis leading to acute liver failure in cases of metastatic liver disease. However, liver hypoxia cannot explain all the reported cases and was never due to circulatory failure from cardiac or septic causes, but to the sinusoidal involvement by tumor cells.
authors.affiliation: Département d'Hépato-Gastroentérologie, Hôpital de Jolimont, Haine-Saint-Paul, Belgique.
authors.forename: J
authors.initials: J
authors.lastname: Henrion
authors.forename: M
authors.initials: M
authors.lastname: Hautekeete
authors.forename: R
authors.initials: R
authors.lastname: Brenard
authors.forename: M
authors.initials: M
authors.lastname: Schapira
authors.forename: G
authors.initials: G
authors.lastname: Somers
authors.forename: A
authors.initials: A
authors.lastname: Geubel
authors.forename: A
authors.initials: A
authors.lastname: Schmitz
authors.forename: R
authors.initials: R
authors.lastname: Gerard
authors.forename: J
authors.initials: J
authors.lastname: Rahier
authors.forename: A
authors.initials: A
authors.lastname: Hoorens
authors.forename: G
authors.initials: G
authors.lastname: Klöppel
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D006501:Hepatic Encephalopathy / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D000860:Hypoxia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008099:Liver / Q000473:pathology*; D008113:Liver Neoplasms / Q000473:pathology / Q000503:physiopathology / Q000556:secondary*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies