Serum levels of tumor necrosis factor‐α correlate with severity of hepatic encephalopathy due to chronic liver failure

Odeh, Majed; Sabo, Edmond; Srugo, Isaac; Oliven, Arie

doi:10.1111/j.1478-3231.2004.0894.x

Cited by 101 publications

(86 citation statements)

References 20 publications

(32 reference statements)

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“…IL-6 and TNF-α are also thought to be involved [14,31,32] and both are able to increase NOx levels. In our study there were no differences at all between the groups and also patients with bleeding had no difference in these cytokine levels compared to patients with other forms of decompensation.…”

Section: Discussionmentioning

confidence: 99%

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Elsing¹

2007

WJG

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AIM:To evaluate plasma levels of nitrite/nitrate (NOx), soluble Fas (sFas) antigen, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in patients with compensated and acute decompensated cirrhosis and to evaluate mediators causing acute decompensation in liver cirrhosis. METHODS:This prospective study was conducted in the medical intensive care unit of an academic tertiary center. Fifty-five patients with acute decompensation (gastrointestinal hemorrhage, encephalopathy, hydropic decompensation) and twenty-five patients with compensated liver cirrhosis were included. Blood samples were taken for analyses of sFas, Nox, IL-6, TNF-α. Liver enzymes and kidney functions were also tested. RESULTS:In patients with acute decompensation, plasma sFas levels were higher than in non-decompensated patients (15 305 ± 4646 vs 12 458 ± 4322 pg/mL, P < 0.05). This was also true for the subgroup of patients with alcoholic liver cirrhosis (P < 0.05). The other mediators were not different and none of the parameters predicted survival, except for ALT (alanine-aminotransferase). In patients with portal-hypertension-induced acute hemorrhage, NOx levels were significantly lower than in patients with other forms of decompensation (70.8 ± 48.3 vs 112.9 ± 74.9 pg/mL, P < 0.05). When NOx levels were normalized to creatinine levels, the difference disappeared. IL-6, TNF-α and sFas were not different between bleeders and non-bleeders. In decompensated patients sFas, IL-6 and NOx levels correlated positively with creatinine levels, while IL-6 levels were dependent on Child class. CONCLUSION:In acute decompensated cirrhotic patients sFas is increased, suggesting a role of apoptosis in this process and patients with acute bleeding have lower NOx levels. However, in this acute complex clinical situation, kidney function seems to have a predominant influence on mediator levels.

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Section: Discussionmentioning

confidence: 99%

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Elsing¹

2007

WJG

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“…TNF-a is a macrophage derived cytokine, produced in large amounts in response to endotoxin. High AF levels of this cytokine have been observed in our patients with SBP [11,16,17]. Since SBP is considered to be the consequence of repeated episodes of bacteremia following intestinal bacterial translocation with seeding of AF, it might be considered that the intermittent presence of bacteria in blood may be followed by an activation of the cytokine cascade [11].…”

Section: Discussionmentioning

confidence: 99%

Alterations in cytokine measurements in ascitic fluid of cirrhotic patients with and without spontaneous bacterial peritonitis

Lagadinou¹,

Solomou²,

Mouzaki³

et al. 2014

Clin Hepatol Hepat Rep

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Aim: To determine the pattern of cytokine synthesis in the ascitic fluid (AF) of cirrhotic patients, with or without spontaneous bacterial peritonitis (SBP). Patients and methods: We prospectively studied 13 cirrhotic patients with ascites, who were admitted at the University Hospital of Patras from May 2008 to December 2009. Patients were separated into two groups: (a) group 1: patients SBP (n=7) (b) group 2: patients without SBP (n=6). Cirrhosis was diagnosed on the basis of typical clinical, laboratory, ultrasonographic findings and/ or liver biopsy. Upon admission a paracentesis of ascetic fluid was performed. Ascitic levels of IL-1b, IL-1ra, IL-6, IL-10, TNFa, sTNFRI and sTNFRII were measured by using an ELISA method. Data are presented as absolute numbers (mean±standard deviation) and were compared using t test. A P value <0.05 was considered significant. Results: Most patients, who were prospectively included in this study and were admitted to the hospital, were males and had cirrhosis due to alcohol abuse. The second cause of cirrhosis in this population was virus hepatitis (B, C or both). The middle age was 69±12 years and 62±15 years for Group 1 and Group 2 respectively. Multivariate analysis of proinflammator and antiinflammatory cytokines showed significant (P<0.05) differences in the levels of sTNFRII and IL-1ra between the two groups of patients (group 1: cirrhotics with SBP vs group 2: cirrhotics without SBP). Ascitic levels of IL-10, IL-6, IL-1ra, TNF-a, STNFRII and STNFRI were higher in ascitic fluid of patients with bacterial ascites, while TGF-b1 levels were lower in the ascitic fluid of patients with SBP (differences not significant). It is remarkable that IL-1b was not expressed in patients either with or without spontaneous bacterial peritonitis SBP. Conclusions:We demonstrated an increased cytokine production in ascitic fluid of cirrhotic patients with SBP, while the levels of anti-inflammatory cytokines sTNFRII and IL-1ra are significantly increased in SBP. It seems, therefore, that an ascitic fluid antiinflammatory response is characteristic in SBP, and this might compromise the final outcome.

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“…Fourth, intestinal bacterial overgrowth and bacterial translocation are increased in cirrhosis [21] . Besides endotoxins, the other possible factors stimulating NO production include cytokines such as TNF-α, IL-1, IL-6, and IFN-γ [22][23][24] Among these, TNF-α has been studied the most. LopezTalavera et al found that anti-TNF-α antibody increases mean arterial pressure and systemic vascular resistance, and decreases cardiac index and portal pressure [25] .…”

Section: Endocannabinoidsmentioning

confidence: 99%

Cardiac and vascular changes in cirrhosis: Pathogenic mechanisms

Liu

Gaskari²,

Lee

2006

WJG

130

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Cardiovascular abnormalities accompany both portal hypertension and cirrhosis. These consist of hyperdynamic circulation, defined as reduced mean arterial pressure and systemic vascular resistance, and increased cardiac output. Despite the baseline increased cardiac output, ventricular inotropic and chronotropic responses to stimuli are blunted, a condition known as cirrhotic cardiomyopathy. Both conditions may play an initiating or aggravating pathogenic role in many of the complications of liver failure or portal hypertension including ascites, variceal bleeding, hepatorenal syndrome and increased postoperative mortality after major surgery or liver transplantation. This review briefly examines the major mechanisms that may underlie these cardiovascular abnormalities, concentrating on nitric oxide, endogenous cannabinoids, central neural activation and adrenergic receptor changes. Future work should address the complex interrelationships between these systems.

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Serum levels of tumor necrosis factor‐α correlate with severity of hepatic encephalopathy due to chronic liver failure

Abstract: Serum levels of TNF correlate positively with the severity of HE in patients with chronic liver failure.

Cited by 101 publications

References 20 publications

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Alterations in cytokine measurements in ascitic fluid of cirrhotic patients with and without spontaneous bacterial peritonitis

Cardiac and vascular changes in cirrhosis: Pathogenic mechanisms

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