Brief Article
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World J Gastroenterol. Mar 7, 2014; 20(9): 2374-2382
Published online Mar 7, 2014. doi: 10.3748/wjg.v20.i9.2374
Procalcitonin, and cytokines document a dynamic inflammatory state in non-infected cirrhotic patients with ascites
Bashar M Attar, Christopher M Moore, Magdalena George, Nicolae Ion-Nedelcu, Rafael Turbay, Annamma Zachariah, Guiliano Ramadori, Jawed Fareed, David H Van Thiel
Bashar M Attar, Rafael Turbay, Annamma Zachariah, Division of Gastroenterology and Hepatology, John H Stroger Hospital of Cook County, Chicago, IL 60612, United States
Bashar M Attar, Christopher M Moore, Magdalena George, David H Van Thiel, Division of Gastroenterology and Hepatology, Rush University Medical Center, Chicago, IL 60612, United States
Nicolae Ion-Nedelcu, Division of Gastroenterology and Hepatology, Victor Babes Infectious Clinic, 050094 Bucharest, Romania
Guiliano Ramadori, Division of Gastroenterology and Hepatology, August Georg University, D-37075 Gottingen, Germany
Jawed Fareed, Division of Gastroenterology and Hepatology, Loyola University Medical Center, Maywood, IL 60153, United States
Author contributions: Attar BM contributed to study design, literature search, patient identification, data collection, data analysis, and manuscript writing; Moore CM contributed to data collection and manuscript writing; George M contributed to study design, laboratory work, data collection, data analysis, and manuscript writing; Ion-Nedelcu N contributed to study design and data analysis; Turbay R contributed to identification of patients with ascites and data collection; Zachariah A contributed to identification of patients with ascites and data collection; Ramadori G contributed to study design and data analysis; Fareed J contributed to study design and data analysis; Van Thiel DH contributed to study hypothesis, study design, data collection, data analysis, and manuscript writing.
Correspondence to: Bashar M Attar, MD, PhD, AGAF, FACP, FACG, FASGE, Professor of Medicine, Division of Gastroenterology and Hepatology, John H Stroger Hospital of Cook County, 1901 W. Harrison Street, Admin. bldg, Suite 1450, Chicago, IL 60612, United States. battar@rush.edu
Telephone: +1-312-8647213 Fax: +1-312-8649214
Received: February 26, 2013
Revised: April 23, 2013
Accepted: June 1, 2013
Published online: March 7, 2014
Abstract

AIM: To quantitate the simultaneous serum and ascitic fluid levels of procalcitonin and inflammatory markers in cirrhotics with and without ascites.

METHODS: A total of 88 consecutive severe cirrhotic patients seen in a large city hospital liver clinic were studied and divided into two groups, those with and without ascites. Group 1 consisted of 41 cirrhotic patients with massive ascites, as demonstrated by necessity for therapeutic large-volume paracentesis. Group 2 consisted of 47 cirrhotic patients without any clinically documented ascites to include either a recent abdominal computed tomography scan or ultrasound study. Serum and ascitic fluid levels of an array of inflammatory markers, including procalcitonin, were measured and compared to each other and a normal plasma panel (NPP).

RESULTS: The values for inflammatory markers assayed in the serum of Groups 1 and 2, and ascitic fluid of the Group 1. The plasma levels of the inflammatory cytokines interleukin (IL)-2, IL-4, IL-6, IL-8, interferon gamma (IFNγ) and epidermal growth factor (EGF) were all significantly greater in the serum of Group 1 as compared to that of the serum obtained from the Group 2 subjects (all P < 0.05). There were significantly greater serum levels of IL-6, IL-8, IL-10, monocyte chemoattractant protein-1, tumor necrosis factor-α, vascular endothelial growth factor and EGF when comparing Group 2 to the NPP. There was no significant difference for IL-1A, IL-1B, IL-2, IL-4 and IFNγ levels between these two groups. Serum procalcitonin levels were increased in cirrhotics with ascites compared to cirrhotics without ascites, but serum levels were similar to ascites levels within the ascites group. Furthermore, many of these cytokines, but not procalcitonin, demonstrate an ascites-to-serum gradient. Serum procalcitonin does not demonstrate any significant difference segregated by liver etiology in the ascites group; but ascitic fluid procalcitonin is elevated significantly in cardiac cirrhosis/miscellaneous subgroup compared to the hepatitis C virus and alcoholic cirrhosis subgroups.

CONCLUSION: Procalcitonin in the ascitic fluid, but not in the serum, differentiates between cirrhotic subgroup reflecting the dynamic interplay of ascites, bacterial translocation and the peri-peritoneal cytokine.

Keywords: Ascites, Bacterial translocation, Inflammatory markers, Procalcitonin, Cirrhosis

Core tip: Procalcitonin received much attention as a serum marker in differentiating sepsis from systemic inflammatory response syndrome and bacterial sepsis. Procalcitonin significance in assessing ascitic fluid inflammation and/or infection is less well characterized. This study demonstrates that non-infected cirrhotics with ascites vs those without ascites manifest peri-peritoneal based immune response mediated by a constellation of pro- and anti-inflammatory protein markers and procalcitonin. This peri-peritoneal response is distinct from the systemic immune response to the underlying hepatic disease process. Its recognition can potentially determine the likelihood for future adverse events like spontaneous bacterial peritonitis, the hepato-renal syndrome and impending death.