Cirrhosis and Liver Failure
No difference in portal and hepatic venous bacterial DNA in patients with cirrhosis undergoing transjugular intrahepatic portosystemic shunt insertion
Version of Record online: 14 JUN 2013
© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Volume 33, Issue 9, pages 1309–1315, October 2013
How to Cite
Liver Int. 2013; 33:1309–1315
- Issue online: 8 SEP 2013
- Version of Record online: 14 JUN 2013
- Accepted manuscript online: 9 MAY 2013 01:53AM EST
- Manuscript Accepted: 2 MAY 2013
- Manuscript Revised: 17 APR 2013
- Manuscript Received: 13 JAN 2013
- L.F. Foght's Foundation
- Hvidovre Hospitals' Research Foundation
- Hvidovre Hospitals Foundation for Liver Diseases
- Novo Nordisk Foundation
- The Capital Region of Denmark
- Foundation for Health Research
- bacterial DNA;
- bacterial translocation;
- lipopolysaccharide-binding protein;
- liver disease;
- polymerase chain reaction;
- portal hypertension;
- transjugular intrahepatic portosystemic shunt
Bacterial translocation (BT) with immune activation may lead to hemodynamical alterations and poor outcomes in patients with cirrhosis.
We investigated bacterial DNA (bDNA), a marker of BT, and its relation to portal pressure and markers of inflammation in the portal and hepatic veins in patients with cirrhosis undergoing TIPS insertion.
We analysed plasma for bDNA and markers of inflammation in 28 patients [median portal pressure gradient 15 (11-19) mmHg] during TIPS treatment for refractory ascites (n = 19) or acute variceal bleeding (n = 9). Advanced cirrhosis was present in the majority [Child–Pugh class (A/B/C): 1/14/13], and most often caused by alcohol (n = 21).
bDNA was detectable in one or both samples in 16 of 28 patients (57%).
bDNA was present in 39% of the samples from the portal vein vs 43% of the samples in the hepatic vein (P = 0.126). Antibiotics had no effect on bDNA or markers of inflammation. Markers of inflammation did not differ between the hepatic and portal veins with the exceptions of soluble urokinase plasminogen activating receptor (suPAR) and vascular endothelial growth factor (VEGF), both higher in the hepatic vein (P = 0.031 and 0.003 respectively).
No transhepatic gradient of bDNA was evident, suggesting that no major hepatic elimination of bDNA occurs in advanced liver disease. bDNA, in contrast to previous reports was largely unrelated to a panel of markers of inflammation and without relation to portal pressure.