The systemic inflammatory response syndrome in cirrhotic patients: Relationship with their in-hospital outcome☆
Introduction
There is growing evidence that systemic inflammation is quite frequent in patients with advanced cirrhosis and portal hypertension, and might be associated with a negative outcome [1]. Systemic inflammation can be caused by overt or occult bacterial infection and can affect clotting function [2], [3]. In cirrhotic patients inflammation has been shown to favor serious complications such as variceal bleeding, encephalopathy and acute-on-chronic liver failure [4]. Accordingly, Thabut et al. [1] showed that inflammation increases the risk of complications and death in cirrhotic patients with acute renal damage.
Excluding hepatocellular carcinoma (HCC), the in-hospital outcome of patients with advanced cirrhosis is mainly driven by liver and/or renal dysfunction [5], [6]. In this setting the role of systemic inflammation has been poorly investigated, even if inflammation can affect both renal and hepatic function.
The aim of this prospective study was to determine (i) the prevalence of systemic inflammation in a cohort of cirrhotic patients consecutively admitted to a tertiary referral centre, (ii) its relationship with liver and kidney function, and (iii) its relationship with the in-hospital outcome. The main endpoints were death and development of portal hypertension-related complications.
Section snippets
Patients
Cirrhotic patients consecutively admitted to our ward from February to September 2004 were enrolled in this study. Inclusion criteria were diagnosis of cirrhosis based on liver biopsy or on obvious clinical, biochemical and imaging features. Exclusion criteria were age <18 years; ongoing cardiac failure (NYHA classes II–IV); organic kidney disease; treatment for chronic obstructive pulmonary disease; diagnosis of HCC or of extrahepatic malignancy; human immunodeficiency virus-positivity; use of
Patients
One hundred and fifty-nine cirrhotic patients were consecutively admitted to hospital. Eighteen patients were excluded according to the study criteria (12 patients with HCC; 2 patients with organic kidney disease; 1 patient with cardiac failure; 1 patient with severe chronic obstructive pulmonary disease; 2 patients with extrahepatic malignancy). The remaining 141 patients were enrolled. They were 100 males and 41 females, with a mean age of 60 ± 14 years. Most patients had severe liver disease
Discussion
This study shows that: (i) SIRS is a relatively frequent event in patients admitted to a tertiary referral centre because of complications due to cirrhosis; (ii) SIRS in cirrhotic patients is closely related to severity of liver disease as shown by the relationship with serum bilirubin, INR, jaundice and MELD score; (iii) SIRS predicts the development of portal hypertension-related complications; (iv) SIRS adversely affect the in-hospital cirrhotic survival.
According to these findings and to
Acknowledgement
Elena Dionigi received a grant form COPEV (Associazione per la Prevenzione e Cura dell’Epatite Virale “Beatrice Vitiello”).
References (37)
- et al.
Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference
Chest
(1992) - et al.
Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document
J Hepatol
(2000) - et al.
A model to predict survival in patients with end-stage liver disease
Hepatology
(2001) Evolving consensus in portal hypertension. Report of the Baveno IV consensus workshop on methodology of diagnosis and therapy in portal hypertension
J Hepatol
(2005)- et al.
Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club
Hepatology
(1996) - et al.
Bacterial infection in patients with advanced cirrhosis: a multicentre prospective study
Dig Liver Dis
(2001) - et al.
Relation of renal impairment and hemorrhagic diathesis to endotoxemia in fulminant hepatic failure
Lancet
(1974) - et al.
Bacterial translocation of enteric organisms in patients with cirrhosis
J Hepatol
(2001) - et al.
Increased lipopolysoccharide binding protein in cirrhotic patients with marked immune and hemodynamic derangement
Hepatology
(2003) - et al.
Tumor necrosis factor-alpha expression by activated monocytes and altered T-cell homeostasis in ascitic alcoholic cirrhosis: amelioration with norfloxacin
J Hepatol
(2004)
Upregulation of TNF-α production signaling pathways in monocytes from patients with advanced cirrhosis: possible role of Akt and IRAK-M
J Hepatol
Bacterial infection in the pathogenesis of variceal bleeding
Lancet
Infection and the progression of hepatic encephalopathy in acute liver failure
Gastroenterology
Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis
J Hepatol
The systemic inflammatory response syndrome in acute liver failure
Hepatology
Liver derived pro-inflammatory cytokines may be important in producing intracranial hypertension in acute liver failure
J Hepatol
Upper gastrointestinal bleeding in patients with hepatic cirrhosis: clinical course and mortality prediction
Am J Gastroenterol
Albumin dialysis reduces portal pressure acutely in patients with severe alcoholic hepatitis
J Hepatol
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The authors declared that they do not have anything to disclose regarding funding from industries or conflict of interest with respect to this manuscript.