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

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.