The systemic inflammatory response syndrome (SIRS) in cirrhotic patients: Relationship with the in-hospital outcome

Department of Internal Medicine, IRCCS Policlinico San Donato, University of Milan, 20097 San Donato Milanese, Milan, Italy.
Journal of Hepatology (Impact Factor: 11.34). 05/2009; 51(3):475-82. DOI: 10.1016/j.jhep.2009.04.017
Source: PubMed


Some evidence suggests that the systemic inflammatory response syndrome (SIRS) contributes to the poor outcome of cirrhotic patients. We studied 141 cirrhotic patients consecutively admitted to a tertiary referral centre assessing prevalence of SIRS and its relationship with in-hospital outcome.
Presence of SIRS was assessed on admission and during hospital stay. Main clinical outcomes were death and development of portal hypertension-related complications.
Thirty-nine patients met SIRS criteria. SIRS was present on admission in 20 of 141 patients (14.1%), whereas it occurred during hospital stay in 19 of 121 (15.7%). SIRS was correlated with bacterial infection at admission (p=0.02), jaundice (p=0.011), high serum creatinine levels (p=0.04), high serum bilirubin levels (p=0.002), high international normalized ratio (p=0.046), high model of end-stage liver disease (MELD) score (p=0.001), and high SOFA score (p=0.003). During a follow-up of 14+/-8 days, 16 patients died (11%), 7 developed portal hypertension-related bleeding (5%), 16 hepatic encephalopathy (11%), and 5 hepatorenal syndrome type-1 (3.5%). SIRS was correlated both to death (p<0.001) and to portal hypertension-related complications (p<0.001). On multivariate analysis, SIRS and MELD were independently associated with death.
SIRS frequently occurs in patients with advanced cirrhosis and is associated with a poor outcome.

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    • "Although some studies on SBP have evaluated prognostic factors such as renal insufficiency, type of organism, bacteremia, and MELD score [23]–[31], no standard marker has been determined to predict SBP mortality. CRP [32] and SIRS [33] are common diagnostic parameters suggested for use as prognostic markers for SBP, but their values diminish when considering cirrhotic patients [6]. Although DNI has been suggested to predict mortality in other infectious conditions [12]–[15], [34], no reports have estimated the prognostic value of DNI in cirrhotic patients with SBP. "
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    ABSTRACT: Spontaneous bacterial peritonitis (SBP) is a common and life-threatening infection in patients with advanced cirrhosis. The prognostic value of a novel marker, the delta neutrophil index (DNI), was investigated relative to mortality in patients with SBP. Seventy-five patients with SBP were studied from April 2010 to May 2012. DNI at initial diagnosis of SBP was determined and compared with 30-day mortality rates. Of the patients, 87.7% were men, and the median age of all patients was 59.0 yrs. The area under the receiver-operating characteristic (ROC) curve of DNI for 30-day mortality was 0.701 (95% confidence interval [CI], 0.553-0.849; p = 0.009), which was higher than that of C-reactive protein (0.640, 95% CI, 0.494-0.786; p = 0.076) or the model for end-stage liver disease score (0.592, 95% CI, 0.436-0.748; p = 0.235). From the ROC curve, with the sum of sensitivity and specificity, the cutoff value of DNI was determined to be 5.7%. In the high-DNI group (DNI ≥5.7%), septic shock and 30-day mortality were more prevalent compared with the low-DNI group (84.2% vs. 48.2%, p = 0.007; 57.9% vs. 14.3%, p<0.001, respectively). Patients with an elevated DNI had a higher risk of 30-day mortality compared with those with a low DNI (4.225, 95% CI, 1.631-10.949; p = 0.003). A higher DNI at the time of SBP diagnosis is an independent predictor of 30-day mortality in patients with SBP.
    PLoS ONE 01/2014; 9(1):e86884. DOI:10.1371/journal.pone.0086884 · 3.23 Impact Factor
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    • "The additional main finding of this study is that a high SIRS score was predictive of HE in dogs with a cPSS. This finding is consistent with studies in humans with liver disease and HE [36-39]. The mechanism by which a SIRS may influence the development of HE is unclear although the presence of a SIRS has been shown to exacerbate the neuropsychological effects of induced hyperammonemia in humans [14]. "
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    ABSTRACT: Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with liver disease. The pathogenesis of he is incompletely understood although ammonia and inflammatory cytokines have been implicated as key mediators. To facilitate further mechanistic understanding of the pathogenesis of HE, a large number of animal models have been developed which often involve the surgical creation of an anastomosis between the hepatic portal vein and the caudal vena cava. One of the most common congenital abnormalities in dogs is a congenital portosystemic shunt (cpss), which closely mimics these surgical experimental models of HE. Dogs with a cPSS often have clinical signs which mimic clinical signs observed in humans with HE. Our hypothesis is that the pathogenesis of HE in dogs with a cPSS is similar to humans with HE. The aim of the study was to measure a range of clinical, haematological and biochemical parameters, which have been linked to the development of HE in humans, in dogs with a cPSS and a known HE grade. One hundred and twenty dogs with a cPSS were included in the study and multiple regression analysis of clinical, haematological and biochemical variables revealed that plasma ammonia concentrations and systemic inflammatory response syndrome scores predicted the presence of HE. Our findings further support the notion that the pathogenesis of canine and human HE share many similarities and indicate that dogs with cPSS may be an informative spontaneous model of human HE. Further investigations on dogs with cPSS may allow studies on HE to be undertaken without creating surgical models of HE thereby allowing the number of large animals used in animal experimentation to be reduced.
    PLoS ONE 01/2014; 9(1):e82303. DOI:10.1371/journal.pone.0082303 · 3.23 Impact Factor
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    • "In ACLF, the systemic inflammatory response is closely tied to its clinical outcomes [19]. The final common pathway leading to acute deterioration of liver function and multi-organ failure appears to be an exaggerated activation of systemic inflammation [20]. "
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    ABSTRACT: Acute-on-chronic liver failure (ACLF) is an acute deterioration of established liver disease. Blocking the TNF (tumor necrosis factor)/TNFR (tumor necrosis factor receptor) 1 pathway may reduce hepatocyte apoptosis/necrosis, and subsequently decrease mortality during development of ACLF. We demonstrated that a long-acting TNF antagonist (soluble TNF receptor: IgG Fc [sTNFR:IgG-Fc]) prevented/reduced development of acute liver failure by blocking the TNF/TNFR1 (TNFRp55) pathway. However, it is still unclear if sTNFR:IgG-Fc can inhibit hepatocyte damage during development of ACLF. Chronic liver disease (liver fibrosis/cirrhosis) was induced in Wistar rats by repeatedly challenging with human serum albumin (HSA), and confirmed by histopathology. ACLF was induced with D-galactosamine (D-GalN)/lipopolysaccharide (LPS) i.p. in the rats with chronic liver disease. Serum and liver were collected for biochemical, pathological and molecular biological examinations. Reduced mortality was observed in sTNFR:IgG-Fc treated ACLF rats, consistent with reduced interleukin (IL)-6 levels in serum and liver, as well as reduced hepatic caspase-3 activity, compared to that of mock treated group. Reduced hepatic damage was confirmed with histopathology in the sTNFR:IgG-Fc treated group, which is consistent with reduced Bcl-2 and Bax, at mRNA and protein levels, but increased hepatocyte proliferation (PCNA). This is also supported by the findings that caspase-3 production was up-regulated significantly in ACLF group compared to the mock treated group. Moreover, up-regulated caspase-3 was inhibited following sTNFR:IgG-Fc treatment. Finally, there was up-regulation of hepatic IL-22R in sTNFR:IgG-Fc treated ACLF rats. sTNFR:IgG-Fc improved survival rate during development of ACLF via ameliorating liver injury with a potential therapeutic value.
    PLoS ONE 07/2013; 8(7):e68757. DOI:10.1371/journal.pone.0068757 · 3.23 Impact Factor
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