Macrophage activation marker, soluble CD163, is an independent predictor of short‐term mortality in patients with cirrhosis and bacterial infection

Abstract

Background & Aims Innate immune system dysfunction is common in advanced cirrhosis, with a central role of the monocyte/macrophage system. Monocytes and macrophages express the scavenger receptor CD163, which is regulated by inflammatory mediators. Cleavage of the receptor leads to the formation of soluble (s)CD163 that represents an anti‐inflammatory response. We aimed to study the clinical importance of sCD163 in cirrhosis. Methods Sera of 378 patients were assayed for sCD163 by ELISA [193 outpatients and 185 patients with acute decompensation (AD)]. A 5‐year follow‐up observational study was conducted to assess the possible association between sCD163 level and poor disease outcomes. Results sCD163 level was associated with disease severity, but not with the presence of varices or prior variceal bleeding. In outpatients, sCD163 level did not predict the development of disease‐specific complications or the long‐term mortality. In patients with AD episode, sCD163 level was significantly higher compared to outpatients but only in the presence of bacterial infection (INF) (AD‐INF:4586, AD‐NON‐INF:3792 and outpatients: 3538 ng/ml, P < 0.015 and P = 0.001, respectively). sCD163 level gradually increased according to severity of infection. During bacterial infections, high sCD163 level (>7000 ng/ml) was associated with increased mortality rate (42% vs. 17%, P < 0.001) and was identified as an independent predictor of 28‐day mortality (hazard ratio:2.96, 95% confidence intervals:1.27–6.95) in multivariate Cox‐regression model comprising aetiology, co‐morbidity, model for end‐stage liver disease score and leucocyte count as covariates. Conclusions High sCD163 level is useful to identify patients with high‐risk of death during an AD episode complicated by bacterial infection. This finding serves as an additional hint towards the significance of anti‐inflammatory response during bacterial infection.

Presepsin teardown - pitfalls of biomarkers in the diagnosis and prognosis of bacterial infection in cirrhosis

“…Some reports also highlighted differences in circulating cytokine levels in bloodstream infections according to Gram specificity, i.e ., Gram-negative infections leaded to higher increase in the level of interleukin (IL)-6, TNF-alpha or IL-10[46]. On the contrary, levels of other APPs, such as C-reactive protein, soluble (s)CD14, sCD163 or soluble urokinase plasminogen activator receptor (SuPAR) are not in relation with the Gram specificity of the infection[47-50]. In the present study, presepsin level was not different according to Gram specificity of the infection, which is in agreement with previous literature findings[51-53].…”

Functional polymorphisms of innate immunity receptors are not risk factors for the non‐SBP type bacterial infections in cirrhosis

“…We performed a cohort study among adult patients with an established diagnosis of cirrhosis of different etiologies, in a tertiary care referral center of Hungary (Division of Gastroenterology Department of Internal Medicine, Clinical Center, University of Debrecen). The present study population is a part of our entire patient cohort comprising a total of 404 patients with cirrhosis who were recruited consecutively between May 1, 2006 and December 31, 2010 from the outpatient clinic during regular, or extraordinary follow‐up visits, and also from the inpatient ward, when hospitalized with an acute decompensation (AD) episode . For the present study, blood samples from 349 patients were available (243 outpatients and 106 hospitalized subjects because of an AD episode; Figure ).…”

Lectin‐complement pathway molecules are decreased in patients with cirrhosis and constitute the risk of bacterial infections

“…We performed a cohort study among adult patients with established diagnosis of cirrhosis of different aetiologies in a tertiary care referral centre of Hungary (Division of Gastroenterology Department of Internal Medicine, Clinical Center, University of Debrecen). This study population is a part of our entire patient cohort comprising a total of 404 patients with cirrhosis and recruited consecutively between 1 May 2006 and 31 December 2010 from the outpatient clinic during regular or extraordinary follow‐up visits and also from the inpatient ward owing to hospitalization with an acute decompensation (AD) episode . The exclusion criteria were (i) if the patient or his/her legal surrogate declined to participate in this study and did not sign the informed consent or (ii) if the patient was sent just for specialist consultation, and followed up regularly elsewhere.…”

“…This study population is a part of our entire patient cohort comprising a total of 404 patients with cirrhosis and recruited consecutively between 1 May 2006 and 31 December 2010 from the outpatient clinic during regular or extraordinary follow-up visits and also from the inpatient ward owing to hospitalization with an acute decompensation (AD) episode. 18 The exclusion criteria were (i) if the patient or his/her legal surrogate declined to participate in this study and did not sign the informed consent or (ii) if the patient was sent just for specialist consultation, and followed up regularly elsewhere. For present study serum samples of 378 patients were available (266 outpatients and 117 hospitalized subjects due to an AD episode).…”