Anemia and Systemic Inflammation Rather than Arterial Circulatory Dysfunction Predict Decompensation of Liver Cirrhosis

Abstract

Background: While systemic inflammation is recognized as playing a central role in the pathogenesis of organ failures in patients with liver cirrhosis, less is known about its relevance in the development of classical hepatic decompensation. Aim: To characterize the relationship between systemic inflammation, hemodynamics, and anemia with decompensation of liver cirrhosis. Methods: This is a post-hoc analysis of a cohort study of outpatients with advanced liver fibrosis or cirrhosis. Results: Analysis included 338 patients of whom 51 patients (15%) were hospitalized due to decompensation of liver cirrhosis during a median follow-up time of six months. In univariate analysis, active alcoholism (p = 0.002), model of end-stage liver disease (MELD) score (p = 0.00002), serum IL-6 concentration (p = 0.006), heart rate (p = 0.03), low arterial blood pressure (p < 0.05), maximal portal venous flow (p = 0.008), and low hemoglobin concentration (p < 0.00001) were associated with hospitalization during follow-up. Multivariate analysis revealed an independent association of low hemoglobin (OR = 0.62, 95% CI = 0.51–0.78, p = 0.001) and serum IL-6 concentration (OR = 1.02, 95% CI = 1.01–1.04, p = 0.03)—but not of hemodynamic parameters—with hepatic decompensation. An inverse correlation between hemoglobin concentration and portal venous flow (R = −0.362, p < 0.0001) was detected for the non-hospitalized patients. Accuracy of baseline hemoglobin levels for predicting hospitalization (AUC = 0.84, p < 0.000001) was high. Conclusion: Anemia and systemic inflammation, rather than arterial circulatory dysfunction, are strong and independent predictors of hepatic decompensation in outpatients with liver cirrhosis.

Early prediction of decompensation (EPOD) score: Non‐invasive determination of cirrhosis decompensation risk

“…HPVG is a marker of portal hypertension, but the invasive procedure is rarely justified in patients with compensated cirrhosis due to the risk of procedural complications. Other studies identified anaemia, markers of systemic inflammation like IL‐6 13 or vitamin D 14 levels as predictors of decompensation. No data on IL‐6 or vitamin D were available in the Explorys cohort but anaemia is indirectly represented by erythrocyte count, haematocrit and haemoglobin concentration.…”

“…However, in patients with compensated cirrhosis, it is difficult to justify invasive HVPG measurement 12 . Other studies identified anaemia, markers of systemic inflammation like IL‐6 13 or vitamin D 14 levels as predictors of decompensation.…”

Recompensation factors for patients with decompensated cirrhosis: a multicentre retrospective case–control study

“…[28][29][30][31][32] Bothou et al found that a low level of haemoglobin was a strongly Open access and independent predictor of hospital admission in outpatients with decompensated liver cirrhosis. 33 The mean value of haemoglobin reported by Bothou et al was 134 g/L. Anaemia can predict the development of ACLF in outpatients with cirrhosis, the median value was 108 g/L.…”

Definition and classification of acute-on-chronic liver diseases

“…LC-A can occur in both compensatory LC (C-LC) and decompensated LC (D-LC). Due to obvious portal hypertension in patients with D-LC, haemodynamic disorders are very likely to occur, causing hepatic tissue ischaemia and hypoxia, and immunodeficiency renders D-LC patients vulnerable to secondary infections, leading to sepsis and further liver injury; thus, D-LC is rarely in a quiescent state[ 55 ]. Therefore, LC-A occurs in patients with C-LC more commonly than in those with D-LC.…”