Original article
Serum levels of C-reactive protein and procalcitonin in critically ill patients with cirrhosis of the liver

https://doi.org/10.1016/j.lab.2005.08.005Get rights and content

Concentrations of C-reactive protein (CRP) and procalcitonin (PCT) have been suggested as markers of infection. The liver is believed to be a key source of CRP and PCT. For this reason we assessed the predictive value of these markers in patients with hepatic cirrhosis in a 31-bed university-hospital department of intensive care. Demographic, clinical, laboratory, and microbiologic data were collected prospectively over 9 months. Of 864 patients included in the study, 79 (9%) had hepatic cirrhosis. Patients with cirrhosis were more likely to have a medical than a surgical admission diagnosis (67 vs 47%, P = .03). They also had a higher rate of infection (48 vs 30%, P = .03) and higher mortality (44 vs 17%, P = .01) than did patients without cirrhosis. We detected no differences in CRP and PCT concentrations among patients with cirrhosis and different disease severity as assessed on the basis of Child-Pugh score. The serum CRP concentration (admission 11.2 ± 4.6 vs 13.0 ± 5.8, maximum 13.9 ± 6.4 vs 18.8 ± 7.3 mg/dL) and PCT (admission 1.3 ± 0.9 vs 2.0 ± 1.4, maximum 3.3 ± 1.8 vs 3.4 ± 2.1 ng/mL) were slightly lower in infected patients with cirrhosis than in infected patients without cirrhosis, but the differences were not statistically significant. Although the liver is considered the main source of CRP and a source of PCT, serum levels of these acute-phase proteins are not significantly lower in patients with cirrhosis than in other patients. Moreover, the predictive power of CRP and PCT for infection was similar for patients with and without cirrhosis.

Section snippets

Methods

We prospectively collected data from all critically ill patients admitted to a 31-bed department of intensive care of a tertiary-care hospital during 3 distinct convenience periods (June-September 2000, June and July 2003, May-July 2004). Demographic, clinical, laboratory, and microbiologic data were collected throughout each patient’s stay. The institution’s ethics committee approved the study, but, because all the parameters assessed were routinely obtained in this department at the time of

Results

We enrolled 864 patients, 79 (9%) of whom had hepatic cirrhosis. Characteristics of the patients are summarized in Table I. Patients with cirrhosis were more likely to have a medical than a surgical admission diagnosis (67% vs 47%, P = .03) and had a higher mortality rate (44% vs 17%, P = .01) than that of patients without cirrhosis. They also had greater disease severity, as assessed on the basis of the APACHE II score, and a greater degree of organ dysfunction, as defined by the SOFA score,

Discussion

Our findings indicate no significant differences in the serum levels of CRP and PCT between patients with and without cirrhosis. Two mechanisms, alone or in combination, may explain these findings: first, that CRP and PCT are, in fact, produced mainly by the liver, and their production is maintained by the hepatocytes in cirrhosis. Three studies demonstrating increased concentrations of CRP in noninfected patients with cirrhosis, regardless of the nature of the cirrhosis (inflammatory or

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      Citation Excerpt :

      In fact, conflicting results exist regarding threshold values and diagnostic accuracy of CRP and PCT in patients with cirrhosis. Bota et al [21], in the evaluation on 79 cirrhotic patients, showed that the serum CRP concentration (admission 11.2 ± 4.6 vs 13.0 ± 5.8, maximum 13.9 ± 6.4 vs 18.8 ± 7.3 mg/dL) and PCT (admission 1.3 ± 0.9 vs 2.0 ± 1.4, maximum 3.3 ± 1.8 vs 3.4 ± 2.1 ng/mL) were slightly lower in infected patients with cirrhosis than in infected patients without cirrhosis, but the differences were not statistically significant. Recently, a new biomarker was introduced.

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