C-reactive protein level as a predictor of mortality in liver disease patients with bacteremia.
Summary of "C-reactive protein level as a predictor of mortality in liver disease patients with bacteremia."
Abstract Background and objective. C-reactive protein (CRP) is synthesized in the liver in response to inflammation, and CRP is a widely used marker of sepsis. In bacteremia the initial CRP level is an independent predictor of mortality. Since the CRP response in patients with chronic liver disease is lower than in patients without liver disease the objective was to assess whether CRP levels in chronic liver disease and bacteremia was associated with case fatality. Patients. The study enrolled 105 patients with chronic liver disease and bacteremia as well as 202 patients with bacteremia and no recorded liver disease from the same region and time period. Methods. Retrospective review of medical records with registration of demography, co-morbidity, bacteriological, biochemical and clinical findings, and Child-Turcotte-Pugh scores. The primary outcome was 30-day mortality. Results. Mortality was significantly higher in patients with chronic liver disease (mortality rate ratio 2.2; 95% confidence interval 1.2-3.9) and it was correlated to Child-Turcotte-Pugh scores. CRP levels were not different between the three Child-Turcotte-Pugh classes (p = 0.33), and no linear correlation with 30-day mortality was observed. Conclusion. Mortality associated with bacteremia is increased in patients with chronic liver disease and it is correlated with Child-Turcotte-Pugh score. The prognostic information of initial CRP levels in patients with chronic liver disease is weak. The clinical management of patients with chronic liver disease and suspected infection should initiate antimicrobial therapy based on clinical, radiological and microbiological findings, whereas the measurement of CRP in bacteremia is less helpful as compared with patients without liver disease.
Department of Infectious Diseases , Aalborg Hospital, Aarhus University Hospital, Aalborg , Denmark.
This article was published in the following journal.
Name: Scandinavian journal of gastroenterology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21905978
- DOI: http://dx.doi.org/10.3109/00365521.2011.615855
Medical and Biotech [MESH] Definitions
The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.
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End Stage Liver Disease
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