The diagnostic and predictive value of ascites nitric oxide levels in patients with spontaneous bacterial peritonitis

Authors

  • Guadalupe Garcia-Tsao,

    Corresponding author
    1. Hepatic Hemodynamic Laboratory, West Haven VA Medical Center, West Haven, CT
    2. Department of Medicine, Liver Center and Digestive Diseases Section, Yale University School of Medicine, New Haven, CT
    • Guadalupe Garcia-Tsao, M.D, Division of Digestive Diseases, Yale University School of Medicine, P.O. Box 3333, New Haven, CT 06510. Fax: (203) 785-7273
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  • Paul Angulo,

    1. Departamento de Gastroenterología, Instituto Nacional de la Nutrición Salvador Zubirán, Mexico City, Mexico
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  • Juan Carlos Garcia,

    1. Hepatic Hemodynamic Laboratory, West Haven VA Medical Center, West Haven, CT
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  • Roberto J. Groszmann,

    1. Hepatic Hemodynamic Laboratory, West Haven VA Medical Center, West Haven, CT
    2. Department of Medicine, Liver Center and Digestive Diseases Section, Yale University School of Medicine, New Haven, CT
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  • Gregory W. Cadelina

    1. Department of Medicine, Liver Center and Digestive Diseases Section, Yale University School of Medicine, New Haven, CT
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Abstract

Nitric oxide (NO) is a messenger molecule involved in pathogen suppression. Cirrhosis is characterized by an increased risk for infections, including spontaneous bacterial peritonitis (SBP). The role of NO in the infections that develop in cirrhosis has not been clearly established. The aim of this study was to investigate the utility of measuring ascites NO in the diagnosis of SBP and/or in determining the predisposition of cirrhotic patients to develop this infection. Nitric oxide metabolites (nitrites + nitrates [NOx]) were measured by chemiluminescence in 105 ascites samples obtained from 87 cirrhotic patients and in 87 simultaneously obtained serum samples. Ascites NO levels were not significantly different among ascites from patients with SBP (n = 39; median, 48 μmol/L), patients with sterile ascites (n = 54; median, 42 μmol/L), and samples obtained after patients with SBP had been treated (n = 12; median, 62 μmol/L). No differences in ascites NO levels were observed between culture-positive and culture-negative peritonitis. Among 50 patients with sterile ascites on initial paracentesis, 7 patients developed peritonitis during follow-up; no differences in baseline NO levels were observed between patients who developed peritonitis (median, 46 μmol/L) and those who did not (median, 41 μmol/L). Among patients with SBP, mortality was significantly higher in those with NO levels >60 μmol/L. A very significant direct correlation was found between ascites and serum NO levels (r2 = .86). In conclusion, ascites NO levels in cirrhotic patients are not useful either to diagnose or to determine predisposition to SBP. Rather, ascites NO levels reflect serum levels, are higher in cirrhotic patients with more severe liver disease, and may be a useful prognostic marker.

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