Admission levels and early changes in serum interleukin‐10 are predictive of poor outcome in acute liver failure and decompensated cirrhosis

Backround & Aim: Immunoparesis contributes to prognosis in acute liver failure (ALF) and decompensated cirrhosis, a phenomenon thought to be mediated by the anti‐inflammatory cytokine interleukin (IL)‐10. We investigated the prognostic value of admission IL‐10 levels and their evolution during the early phase of treatment in intensive care, in comparison to the pro‐inflammatory cytokines IL‐6 and tumour necrosis factor (TNF)‐α. Methods: We measured these cytokines within 48 h of admission in 51 ALF and 39 decompensated cirrhosis patients admitted to intensive care, and obtained follow‐up measurement a median of 2 days later in 35 patients. Results: Levels of all cytokines were higher in those with a poor outcome. IL‐10 performed as well as TNF‐α and IL‐6 in the whole cohort (area under receiver operator curve 0.73 vs 0.66 and 0.72). However IL‐10 outperfomed pro‐inflammatory cytokines in the subgroups with ALF (0.80 vs 0.63 and 0.70) and acetaminophen‐induced ALF (0.92 vs 0.67 and 0.81). Levels of all cytokines rose significantly in non‐surviving patients (n=15); IL‐10 by a factor of 2, TNF‐α by 2.6 and IL‐6 by 1.13. No significant changes were seen in the surviving patients. In ALF, IL‐10 was an independent predictor of outcome in multivariate analysis. Conclusion: The magnitude of the compensatory anti‐inflammatory response at admission, and its development during the early phase of treatment, predicts outcome as well as the pro‐inflammatory response in acute hepatic syndromes and supports a vital role for this immunological phenomenon in the outcome of these patients.