title: Endotoxin and tumor necrosis factor-receptor levels in portal and hepatic vein of patients with alcoholic liver cirrhosis receiving elective transjugular intrahepatic portosystemic shunt.
abstract: OBJECTIVE
  In cirrhosis portal hypertension can promote bacterial translocation and increase serum endotoxin levels. Vice versa, endotoxin aggravates portal hypertension by induction of systemic and splanchnic vasodilation, and by triggering hepatic inflammatory response via tumor necrosis factor α (TNFα). However, the hepatic elimination of endotoxin in cirrhotic patients with severe portal hypertension, in the absence of acute complications, has not been investigated so far.
  
  
  METHODS
  Twenty patients with alcoholic liver cirrhosis received transjugular intrahepatic portosystemic shunt at an event-free interval for either refractory ascites or recurrent bleeding. During the transjugular intrahepatic portosystemic shunt procedure portal and hepatic venous blood samples were obtained and endotoxin levels were measured by a chromogenic limulus-assay. In 16 of these patients an enzyme-linked immunosorbent assay was used to measure levels of the soluble TNFα-receptors sTNF-R55 and sTNF-R75.
  
  
  RESULTS
  Portal venous endotoxin levels correlated with portal vein velocity (P=0.03) and arterial systolic blood pressure (P=0.007). Portal endotoxin levels correlated with portal venous sTNF-R75-levels (P=0.039; r=0.521) and hepatic venous sTNF-R55-levels (P=0.009; r=0.669). Hepatic venous levels of both sTNF-R55 and sTNF-R75 correlated directly with the model for end-stage liver disease-score, and inversely with cholinesterase. However, we did not find significant differences in endotoxin levels nor in sTNF-R55-levels and sTNF-R75-levels between portal and hepatic venous blood.
  
  
  CONCLUSIONS
  Endotoxin levels correlated with hemodynamic derangement in cirrhotic severe portal hypertension, and with levels of soluble TNFα-receptors. Soluble TNFα-receptor levels correlated with the severity of liver dysfunction. However, in this study an endotoxin concentration gradient across the liver was absent, suggesting negligible primary hepatic endotoxin elimination in the absence of complications.
authors.affiliation: Department of Internal Medicine I, University of Bonn, Germany. jonel.trebicka@ukb.uni-bonn.de
authors.forename: Jonel
authors.initials: J
authors.lastname: Trebicka
authors.forename: Aleksander
authors.initials: A
authors.lastname: Krag
authors.forename: Stefan
authors.initials: S
authors.lastname: Gansweid
authors.forename: Beate
authors.initials: B
authors.lastname: Appenrodt
authors.forename: Peter
authors.initials: P
authors.lastname: Schiedermaier
authors.forename: Tilman
authors.initials: T
authors.lastname: Sauerbruch
authors.forename: Ulrich
authors.initials: U
authors.lastname: Spengler
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D004731:Endotoxins / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D006503:Hepatic Veins / Q000378:metabolism; D006801:Humans; D006975:Hypertension, Portal / Q000097:blood; D008104:Liver Cirrhosis, Alcoholic / Q000097:blood* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D011169:Portal Vein / Q000378:metabolism; D019168:Portasystemic Shunt, Transjugular Intrahepatic; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood; D018608:Ultrasonography, Doppler / Q000379:methods
chemical_list: D004731:Endotoxins; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II