Brief Article
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World J Hepatol. Feb 27, 2014; 6(2): 85-91
Published online Feb 27, 2014. doi: 10.4254/wjh.v6.i2.85
Disease dependent qualitative and quantitative differences in the inflammatory response to ascites occurring in cirrhotics
Bashar M Attar, Magdalena George, Nicolae Ion-Nedelcu, Guilliano Ramadori, David H Van Thiel
Bashar M Attar, Division of Gastroenterology and Hepatology, John H Stroger Hospital of Cook County, Chicago, IL 60612, United States
Bashar M Attar, Magdalena George, David H Van Thiel, Rush University Medical Center, Chicago, IL 60612, United States
Nicolae Ion-Nedelcu, Victor Babes Infectious and Tropical Disease Clinic, 70346 Bucharest, Romania
Guilliano Ramadori, Department of Gastroenterology and Endocrinology, August Georg University, 3400 Gottingen, Germany
Author contributions: Attar BM contributed to literature search, patient identification, and manuscript writing; Van Thiel DH contributed to study hypothesis, data collectionand manuscript writing; all the authors participated in study design and data analysis.
Correspondence to: Bashar M Attar, MD, PhD, AGAF, FACP, FACG, FASGE, Professor, Division of Gastroenterology and Hepatology, John H Stroger Hospital of Cook County, 1901 W. Harrison Street, Cook County-Admin. bldg, Suite 1450, Chicago, IL 60612, United States.
Telephone: +1-312-8647213 Fax: +1-312-8649214
Received: July 4, 2013
Revised: November 25, 2013
Accepted: January 13, 2014
Published online: February 27, 2014
Core Tip

Core tip: Previous studies have examined factors relative to the pathogenesis of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis of the liver. This study was designed to examine the role of cytokines in decompensated cirrhotics requiring a large-volume paracentesis for ascites management and to compare the biomarker responses present in both the plasma and ascitic fluid of cirrhotics of differing etiologies. Factors likely to represent protective cytokines associated with a reduced risk for SBP include epidermal growth factor, tumor necrosis factor-α, interleukin (IL)-1A, IL-8, and IL-10. Those are more likely to be associated with potential for SBP include: IL-1B, IL-4, monocyte chemotactic protein -1, and interfero-γ.