Systemic inflammation is associated with the risk of first non-bleeding, but not bleeding decompensation in patients with compensated cirrhosis

Background The transition from compensated to decompensated cirrhosis indicates a poor prognosis, and decompensated symptoms are subclassified as bleeding and non-bleeding. This study aimed to investigate the association between serum systemic inflammation marker levels and the development of the first bleeding and non-bleeding decompensation in patients with compensated cirrhosis. Methods This retrospective study included 214 patients with compensated liver cirrhosis. The baseline serum C-reactive protein, interleukin 6, procalcitonin, and serum amyloid A protein levels were measured. Factors associated with the first decompensation were assessed using the Cox proportional hazards model. The probability of first decompensation was evaluated using Kaplan–Meier analysis and the log-rank test. Results In the study cohort, 167 (78%) patients showed elevation of one or more systemic inflammation markers. During a median follow-up of 3.6 years, 28 and 35 patients developed first bleeding and non-bleeding decompensation, respectively. The multivariate Cox proportional hazards model identified that nonviral etiology and low platelet count were significantly associated with bleeding decompensation and nonviral etiology, albumin–bilirubin grade, and serum interleukin 6 level with non-bleeding decompensation. Kaplan–Meier analyses showed that patients with high serum interleukin 6 levels (≥ 10 pg/mL) showed significantly higher probability of first non-bleeding decompensation than those with low serum interleukin 6 levels, but probability of bleeding decompensation was not different between them. Conclusion Serum pro-inflammatory cytokine interleukin 6 predicts the risk of first non-bleeding decompensation but not bleeding decompensation in patients with compensated cirrhosis.