Fecal calprotectin is a useful screening parameter for hepatic encephalopathy and spontaneous bacterial peritonitis in cirrhosis

Authors

  • Felix Gundling,

    1. Department of Gastroenterology, Hepatology and Gastrointestinal Oncology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
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  • Fabian Schmidtler,

    1. Department of Cardiology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
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  • Alexander Hapfelmeier,

    1. Institut für medizinische Statistik und Epidemiologie, Technical University of Munich, University of Munich, Munich, Germany
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  • Benjamin Schulte,

    1. Department of Rheumatology and Immunology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
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  • Thomas Schmidt,

    1. Department of Gastroenterology, Hepatology and Gastrointestinal Oncology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
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  • Christian Pehl,

    1. Department of Internal Medicine, Vilsbiburg Hospital, Vilsbiburg, Germany
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  • Wolfgang Schepp,

    1. Department of Gastroenterology, Hepatology and Gastrointestinal Oncology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
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  • Holger Seidl

    1. Department of Gastroenterology, Hepatology and Gastrointestinal Oncology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Munich, Germany
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Dr. med. Felix Gundling, Department of Gastroenterology, Hepatology and Gastrointestinal Oncology, Bogenhausen Academic Teaching Hospital, Technical University of Munich, Englschalkinger Straße 77, 81925 Munich, Germany
Tel: ++49 89 9270 2061
Fax: ++49 89 9270 2486
e-mail: gastroenterologie@kh-bogenhausen.de

Abstract

Objective: Bacterial translocation, causing intestinal inflammation, is one of the key mechanisms in the pathogenesis of hepatic encephalopathy (HE) and spontaneous bacterial peritonitis (SBP) The presence of fecal calprotectin quantitatively relates to intestinal neutrophil migration and is therefore considered as a marker of intestinal inflammation. We aimed to assess the role of fecal calprotectin concentrations (FCCs) in diagnosing the onset and severity of HE and SBP.

Methods: Sixty-one cirrhotics were prospectively included. Forty-two subjects served as controls. Several complications of cirrhosis were diagnosed by reference methods. Stool samples were collected for measuring FCCs. Patients revealing other causes of abnormal calprotectin results, e.g. gastrointestinal bleeding or inflammatory bowel disease were excluded. Multivariate analysis of cirrhosis-associated complications and their relation to FCCs was performed.

Results: Fecal calprotectin concentrations were higher in cirrhotics compared with controls (P<0.001). Among cirrhotics, FCCs were elevated dependent on the severity of liver disease as assessed by Child- and model for end-stage liver disease-scores. The corresponding correlation co-efficients by Spearman's were 0.577 (P<0.001) and 0.303 (P=0.018) respectively. A correlation emerged between elevated FCCs and HE grading as measured by West–Haven criteria and critical flicker frequency (both P<0.001; sensitivity=0.94 and 0.93, specificity=0.95 and 0.89 respectively) and SBP (P<0.02; sensitivity=0.71, specificity=0.79). FCCs were higher in cirrhotic subjects with additional extra-intestinal inflammation (P<0.01; sensitivity=0.65, specificity=0.8). The Pearsons correlation coefficients were 0.190 and 0.164 revealing no influence (P=0.142 and P=0.207) of laboratory parameters of systemic inflammation on FCCs in cirrhotic subgroup.

Conclusions: Fecal calprotectin concentrations serve as a screening tool for HE and SBP. Assessment of FCCs may faciliate grading of HE-severity.

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