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Association of markers of bacterial translocation with immune activation in decompensated cirrhosis

Mortensen, Christiana,b; Jensen, Jørgen Skovd; Hobolth, Lisee; Dam-Larsen, Sannef; Madsen, Bjørn S.g; Andersen, Ovec; Møller, Sørenb; Bendtsen, Flemminga

European Journal of Gastroenterology & Hepatology: December 2014 - Volume 26 - Issue 12 - p 1360–1366
doi: 10.1097/MEG.0000000000000217
Original Articles: Liver Failure

Background: Bacterial translocation (BT) may cause infections, in particular, spontaneous bacterial peritonitis (SBP). In the absence of overt infection, BT may further stimulate the immune system and contribute to haemodynamic alterations and complications. Bacterial DNA (bDNA) is claimed to be a promising surrogate marker for BT, although its clinical relevance has been questioned.

Materials and methods: In 38 cirrhotic patients with and without SBP, bDNA in blood and ascites were assessed by 16S rDNA quantitative PCR. Levels of lipopolysaccharide-binding protein in plasma and highly sensitive C-reactive protein, tumour necrosis factor-α, soluble urokinase plasminogen activating receptor, interleukin-6, interleukin 8, interferon-γ inducible protein-10 and vascular endothelial growth factor in plasma and ascites were measured by multiplex cytokine and ELISA assays.

Results: In patients without signs of SBP or positive cultures, we found a high frequency of bDNA but low concordance of bDNA between blood and ascites. Markers of inflammation were not significantly different between blood bDNA-positive (22%), ascites bDNA-positive (52%), and bDNA-negative patients. The 16S rDNA PCR failed to show bDNA in two out of six samples with SBP. Sequencing of positive samples did not determine the source of bDNA.

Conclusion: bDNA as assessed by this PCR method was largely unrelated to markers of inflammation and does not seem to be of clinical value in the diagnosis of SBP. According to our results, bDNA is not a reliable marker of BT.

Departments of aGastroenterology

bClinical Physiology and Nuclear Medicine, Centre of Functional Imaging and Research

cCentre for Clinical Research, Hvidovre University Hospital, Hvidovre

dMycoplasma Laboratory, Microbiology and Infection Control, Statens Serum Institut

eDepartment of Internal Medicine I, Bispebjerg Hospital

fDepartment of Internal Medicine, Glostrup Hospital, Glostrup

gDepartment of Medicine, Svendborg Sygehus, Svendborg, Denmark

Correspondence to Christian Mortensen, MD, Department of Gastroenterology, Hvidovre University Hospital, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark Tel: +45 38 623 181; fax: +45 3 8623 777; e-mail: c.o.mortensen@gmail.com

Received June 26, 2014

Accepted August 29, 2014

© 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins