Abstract
BackgroundTNFα 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.MethodsForty-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.ResultsBefore 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.ConclusionHepatic venous levels of sTNFR-I after TIPS insertion may predict mortality in patients with severe portal hypertension.
Highlights
Portal hypertension is a major cause of mortality and morbidity in cirrhosis regardless of its aetiology [1,2]
Forty-nine patients with liver cirrhosis and severe portal hypertension referred for transjugular intrahepatic portosystemic shunt (TIPS) insertions were enrolled into the study between May 1994 and March 1999
Clinical and biochemical characteristics of the patients The major clinical and demographic data are summarized in Biochemical parameters
Summary
Portal hypertension is a major cause of mortality and morbidity in cirrhosis regardless of its aetiology [1,2]. TNFa increases the intrahepatic resistance due to activation of macrophages and hepatic stellate cells, whereas it leads to extra-hepatic vasodilation and increased portal-venous inflow through induction of nitric oxide. Taken together, both processes aggravate portal hypertension [5,6,7,8,9,10]. Complications of portal hypertension, such as variceal bleeding or refractory ascites, can be controlled by insertion of a transjugular intrahepatic portosystemic shunt (TIPS) [1,2,33] This procedure allows to simultaneously analyse blood from the portal and hepatic vein, reflecting processes in the intestinal compartment and the liver, respectively.
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