Soluble TNF-alpha-receptors I are prognostic markers in TIPS-treated patients with cirrhosis and portal hypertension

• Published in: PloS one 2013, Vol.8 (12), p.e83341-e83341
• Main Authors: Trebicka, Jonel, Krag, Aleksander, Gansweid, Stefan, Schiedermaier, Peter, Strunk, Holger M, Fimmers, Rolf, Strassburg, Christian P, Bendtsen, Fleming, Møller, Søren, Sauerbruch, Tilman, Spengler, Ulrich
• Format: Article
• Language: English
• Subjects: Adult; Aged; Aged, 80 and over; Ascites; Bile; Biochemical characteristics; Biochemistry; Biology; Biomarkers - blood; Bleeding; Blood; Blood Chemical Analysis; Catheterization; Cirrhosis; Correlation analysis; Enzyme-linked immunosorbent assay; Female; Hemodynamics; Humans; Hypertension; Hypertension, Portal - blood; Hypertension, Portal - etiology; Hypertension, Portal - mortality; Hypertension, Portal - surgery; Insertion; Liver; Liver cirrhosis; Liver Cirrhosis - blood; Liver Cirrhosis - complications; Liver Cirrhosis - mortality; Liver Cirrhosis - surgery; Male; Medicine; Middle Aged; Mortality; Patients; Portal Pressure; Portasystemic Shunt, Transjugular Intrahepatic; Prognosis; Receptors; Receptors, Tumor Necrosis Factor, Type I - blood; Regression analysis; Rodents; Survival; Tips; Tumor necrosis factor receptors; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Veins & arteries
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0083341

TNFα levels are increased in liver cirrhosis even in the absence of infection, most likely owing to a continuous endotoxin influx into the portal blood. Soluble TNFα receptors (sTNFR type I and II) reflect release of the short-lived TNFα, because they are cleaved from the cells after binding of TNFα. The aims were to investigate the circulating levels of soluble TNFR-I and -II in cirrhotic patients receiving TIPS. Forty-nine patients with liver cirrhosis and portal hypertension (12 viral, 37 alcoholic) received TIPS for prevention of re-bleeding (n = 14), therapy-refractory ascites (n = 20), or both (n = 15). Portal and hepatic venous blood was drawn in these patients during the TIPS procedure and during the control catheterization two weeks later. sTNFR-I and sTNFR-II were measured by ELISA, correlated to clinical and biochemical characteristics. Before TIPS insertion, sTNFR-II levels were lower in portal venous blood than in the hepatic venous blood, as well as in portal venous blood after TIPS insertion. No significant differences were measured in sTNFR-I levels. Hepatic venous levels of sTNFR-I above 4.5 ng/mL (p = 0.036) and sTNFR-II above 7 ng/mL (p = 0.05) after TIPS insertion were associated with decreased survival. A multivariate Cox-regression survival analysis identified the hepatic venous levels of sTNFR-I (p = 0.004) two weeks after TIPS, and Child score (p = 0.002) as independent predictors of mortality, while MELD-score was not. Hepatic venous levels of sTNFR-I after TIPS insertion may predict mortality in patients with severe portal hypertension.