Einfluss der systemischen Inflammation für die portalvenöse und systemische Hämodynamik bei Patienten mit Leberzirrhose - Implikationen für hepatische Dekompensation

Systemic inflammation is known to be a key player in the pathogenesis of the development of cirrhosis and consequent liver failure. However, the role of inflammation in the cascade of classical liver decompensation is not fully understood. This research project, part of a series of projects investigating hepatic decompensation in a large cohort of patients, aims to elucidate the interplay between systemic inflammation, hemodynamics, and anemia in decompensation in cirrhosis. The study population consisted of consecutively followed outpatients with advanced liver fibrosis or cirrhosis. We approached our research question by performing a post hoc analysis for potential parameters associated with liver decompensation and/or hospitalization. In total, we analyzed data from 338 patients, with 50/338 (15%) hospitalized for decompensated cirrhosis during a median follow-up of six months. In a first step, we performed a univariate analysis, which showed that 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. Subsequent multivariate analysis showed 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 hemodynamic parameters, with liver decompensation. An inverse correlation between hemoglobin concentration and portal venous flow (R = -0.362, p < 0.0001) was observed in non-hospitalized patients. The accuracy of baseline hemoglobin levels in predicting hospitalization (area under the curve-AUC = 0.84, p < 0.000001) was high. In conclusion, our study showed that anemia and systemic inflammation, but not arterial circulatory dysfunction, are strong and independent predictors of liver decompensation in outpatients with cirrhosis.