Systemic inflammatory response and serum lipopolysaccharide levels predict multiple organ failure and death in alcoholic hepatitis
- PMID: 25761863
- PMCID: PMC4549175
- DOI: 10.1002/hep.27779
Systemic inflammatory response and serum lipopolysaccharide levels predict multiple organ failure and death in alcoholic hepatitis
Abstract
Alcoholic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death. However, the driving factors are largely unknown. At admission, patients with AH often show criteria of systemic inflammatory response syndrome (SIRS) even in the absence of an infection. We hypothesize that the presence of SIRS may predispose to MOF and death. To test this hypothesis, we studied a cohort including 162 patients with biopsy-proven AH. The presence of SIRS and infections was assessed in all patients, and multivariate analyses identified variables independently associated with MOF and 90-day mortality. At admission, 32 (19.8%) patients were diagnosed with a bacterial infection, while 75 (46.3%) fulfilled SIRS criteria; 58 patients (35.8%) developed MOF during hospitalization. Short-term mortality was significantly higher among patients who developed MOF (62.1% versus 3.8%, P < 0.001). The presence of SIRS was a major predictor of MOF (odds ratio = 2.69, P = 0.025) and strongly correlated with mortality. Importantly, the course of patients with SIRS with and without infection was similar in terms of MOF development and short-term mortality. Finally, we sought to identify serum markers that differentiate SIRS with and without infection. We studied serum levels of high-sensitivity C-reactive protein, procalcitonin, and lipopolysaccharide at admission. All of them predicted mortality. Procalcitonin, but not high-sensitivity C-reactive protein, serum levels identified those patients with SIRS and infection. Lipopolysaccharide serum levels predicted MOF and the response to prednisolone.
Conclusion: In the presence or absence of infections, SIRS is a major determinant of MOF and mortality in AH, and the mechanisms involved in the development of SIRS should be investigated; procalcitonin serum levels can help to identify patients with infection, and lipopolysaccharide levels may help to predict mortality and the response to steroids.
© 2015 by the American Association for the Study of Liver Diseases.
Conflict of interest statement
Potential conflict of interest: Nothing to report.
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Comment in
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Alcoholic hepatitis: Can we outwit the Grim Reaper?Hepatology. 2015 Sep;62(3):671-3. doi: 10.1002/hep.27852. Epub 2015 May 26. Hepatology. 2015. PMID: 25891016 Free PMC article.
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Association between systemic inflammatory response syndrome and mortality in alcoholic hepatitis: A meta-analysis.Hepatology. 2016 Aug;64(2):696-7. doi: 10.1002/hep.28366. Epub 2016 Jan 6. Hepatology. 2016. PMID: 26645856 No abstract available.
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Assessing endotoxemia in alcoholic hepatitis.Hepatology. 2016 Aug;64(2):679-80. doi: 10.1002/hep.28629. Epub 2016 Jun 7. Hepatology. 2016. PMID: 27123567 No abstract available.
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Lyso-phosphatidylcholine: A potential metabolomic biomarker for alcoholic liver disease?Hepatology. 2016 Aug;64(2):678-9. doi: 10.1002/hep.28630. Epub 2016 Jun 16. Hepatology. 2016. PMID: 27123871 No abstract available.
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Reply.Hepatology. 2016 Aug;64(2):680-1. doi: 10.1002/hep.28631. Epub 2016 Jun 16. Hepatology. 2016. PMID: 27123989 No abstract available.
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