Immunoparesis contributes to prognosis in acute liver failure and decompensated cirrhosis.
A phenomenon thought to be mediated by the anti-inflammatory cytokine interleukin-10.
Dr Berry and colleagues from the United Kingdom investigated the prognostic value of admission interleukin-10 levels.
In addition, the team evaluated the evolution of interleukin-10 during the early phase of treatment in intensive care in comparison to the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-a.
The team measured these cytokines within 48 hours of admission in 51 acute liver failure and 39 decompensated cirrhosis patients admitted to intensive care, and obtained follow-up measurement a median of 2 days later in 35 patients.
The researchers found that levels of all cytokines were higher in those with a poor outcome.
Interleukin-10 performed as well as tumor necrosis factor-alpha, and interleukin-6 in the whole cohort.
|Interleukin-10 rose by a factor of 2 in non-surviving patients|
However interleukin-10 outperfomed pro-inflammatory cytokines in the subgroups with acute liver failure and acetaminophen-induced acute liver failure.
The research team found that levels of all cytokines rose significantly in non-surviving patients, with interleukin-10 by a factor of 2, tumor necrosis factor -a by 3 and interleukin-6 by 1.1.
The team observed no significant changes in the surviving patients.
In acute liver failure, interleukin-10 was an independent predictor of outcome in multivariate analysis.
Dr Berry's team concluded, “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."
"It supports a vital role for this immunological phenomenon in the outcome of these patients.”