No difference in portal and hepatic venous bacterial <scp>DNA</scp> in patients with cirrhosis undergoing transjugular intrahepatic portosystemic shunt insertion

Mortensen, Christian; Karlsen, Stine; Grønbæk, Henning; Nielsen, Dorte Guldbrand; Frevert, Susanne; Clemmesen, J; Möller, Sören; Jensen, Jørgen Skov; Bendtsen, Flemming

doi:10.1111/liv.12205

Cited by 20 publications

(29 citation statements)

References 27 publications

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“…Intestinal bacterial translocation (BT) is part of this process and may be involved in activation of hepatic macrophages and thus development of cirrhosis and its complications. BT can be estimated by the circulating level of lipopolysaccharide (LPS)‐binding protein (LBP); however, a potential new marker of BT is the presence of bacterial DNA (bDNA) in the blood, which is associated with a poor prognosis in cirrhosis …”

Section: Introductionmentioning

confidence: 99%

The soluble mannose receptor is released from the liver in cirrhotic patients, but is not associated with bacterial translocation

Laursen

Rødgaard‐Hansen

Møller

et al. 2016

Liver International

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This study showed hepatic soluble mannose receptor excretion with a higher level in the hepatic than the portal vein, though with no associations to bacterial DNA. We observed associations between soluble mannose receptor levels and portal pressure and higher levels in patients with acute variceal bleeding indicating the soluble mannose receptor as a marker of complications of cirrhosis, but not bacterial translocation.

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Section: Introductionmentioning

confidence: 99%

The soluble mannose receptor is released from the liver in cirrhotic patients, but is not associated with bacterial translocation

Laursen

Rødgaard‐Hansen

Møller

et al. 2016

Liver International

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“…The authors concluded that no major hepatic elimination of bacterial DNA occurs in advanced liver diseases. Furthermore, the authors demonstrated that bacterial DNA was unrelated to a panel of markers of inflammation and without relation to portal pressure [42]. These divergent results underline the difficulty in investigating and better understanding the mechanisms and consequences of bacterial translocation in liver cirrhosis.…”

Section: Clinical Studiesmentioning

confidence: 99%

“…In this study, LPS-binding protein was measured by limulus amebocyte lysate assay [41]. In another study bacterial DNA was measured in blood from the hepatic vein and the portal vein during a TIPS procedure [42]. No transhepatic gradient of bacterial DNA was observed.…”

Section: Clinical Studiesmentioning

confidence: 99%

Infection as a Trigger for Portal Hypertension

Steib¹,

Schewe²,

Gerbes³

2015

Dig Dis

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Background: Microbial infections are a relevant problem for patients with liver cirrhosis. Different types of bacteria are responsible for different kinds of infections: Escherichia coli and Klebsiella pneumoniae are frequently observed in spontaneous bacterial peritonitis or urinary tract infections, and Streptococcus pneumoniae and Mycoplasma pneumoniae in pulmonary infections. Mortality is up to 4-fold higher in infected patients with liver cirrhosis than in patients without infections. Key Messages: Infections in patients with liver cirrhosis are due to three major reasons: bacterial translocation, immune deficiency and an increased incidence of systemic infections. Nonparenchymal liver cells like Kupffer cells, sinusoidal endothelial cells and hepatic stellate cells are the first liver cells to come into contact with microbial products when systemic infection or bacterial translocation occurs. Kupffer cell (KC) activation by Toll-like receptor (TLR) agonists and endothelial sinusoidal dysfunction have been shown to be important mechanisms increasing portal pressure following intraperitoneal lipopolysaccharide pretreatment in cirrhotic rat livers. Reduced intrahepatic vasodilation and increased intrahepatic vasoconstriction are the relevant pathophysiological pathways. Thromboxane A₂ and leukotriene (LT) C₄/D₄ have been identified as important vasoconstrictors. Accordingly, treatment with montelukast to inhibit the cysteinyl-LT₁ receptor reduced portal pressure in cirrhotic rat livers. Clinical studies have demonstrated that activation of KCs, estimated by the amount of soluble CD163 in the blood, correlates with the risk for variceal bleeding. Additionally, intestinal decontamination with rifaximin in patients with alcohol-associated liver cirrhosis reduced the portal pressure and the risk for variceal bleeding. Conclusions: TLR activation of nonparenchymal liver cells by pathogens results in portal hypertension. This might explain the pathophysiologic correlation between microbial infections and portal hypertension in patients with liver cirrhosis. These findings are the basis for both better risk stratifying and new treatment options, such as specific inhibition of TLR for patients with liver cirrhosis and portal hypertension.

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“…Additionally, it did not accurately predict the presence of SBP [44] . bDNA was also found to be largely unrelated to a panel of markers of inflammation and without association with portal pressure in patients with cirrhosis undergoing transjugular intrahepatic portosystemic shunt insertion [45] . No correlation between detection of bDNA in ascites and SBP was found [46] .…”

Section: Bacterial Dnamentioning

confidence: 98%

“…Rincón et al [39] , Sersté et al [40] , Feng et al [41] , Fujita et al [42] , Vlachogiannakos et al [43] , Mortensen et al [44] , Mortensen et al [45] , Appenrodt et al [46] LPS Gram (-) bacteria Pros: Correlation with TNF-α, stage of cirrhosis, prognostic value for severity of liver damage…”

Section: Bacterial Dnamentioning

confidence: 99%

Markers of bacterial translocation in end-stage liver disease

Koutsounas¹,

Kaltsa²,

Siakavellas³

et al. 2015

WJH

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Bacterial translocation (BT) refers to the passage of viable bacteria or bacterial products from the intestinal lumen, through the intestinal epithelium, into the systemic circulation and extraintestinal locations. The three principal mechanisms that are thought to be involved in BT include bacterial overgrowth, disruption of the gut mucosal barrier and an impaired host defence.BT is commonly observed in liver cirrhosis and has been shown to play an important role in the pathogenesis of the complications of end stage liver disease, including infections as well as hepatic encephalopathy and hepatorenal syndrome. Due to the importance of BT in the natural history of cirrhosis, there is intense interest for the discovery of biomarkers of BT. To date, several such candidates have been proposed, which include bacterial DNA, soluble CD14, lipopolysaccharides endotoxin, lipopolysaccharide-binding protein, calprotectin and procalcitonin. Studies on the association of these markers with BT have demonstrated not only promising data but, oftentimes, contradictory results. As a consequence, currently, there is no optimal marker that may be used in clinical practice as a surrogate for the presence of BT.

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No difference in portal and hepatic venous bacterial DNA in patients with cirrhosis undergoing transjugular intrahepatic portosystemic shunt insertion

Abstract: 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.

Cited by 20 publications

References 27 publications

The soluble mannose receptor is released from the liver in cirrhotic patients, but is not associated with bacterial translocation

The soluble mannose receptor is released from the liver in cirrhotic patients, but is not associated with bacterial translocation

Infection as a Trigger for Portal Hypertension

Markers of bacterial translocation in end-stage liver disease

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