Delayed increase of S100A9 messenger RNA predicts hospital-acquired infection after septic shock

Septic shock remains a serious disease with high mortality and increased risk of hospital-acquired infection. The prediction of outcome is of the utmost importance for selecting patients for therapeutic strategies aiming to modify the immune response. The aim of this study was to assess the capability of S100A9 messenger RNA in whole blood from patients with septic shock to predict survival and the occurrence of hospital-acquired infection.

Cohort study.

Two intensive care units in a university hospital.

The study included patients with septic shock (n = 166) and healthy volunteers (n = 44).

None.

For the patients with septic shock patients, overall mortality was 38% and the mean Simplified Acute Physiologic Scale II on shock onset was 52. Using quantitative reverse transcriptase-polymerase chain reactions, we found that median S100A9 messenger RNA was significantly lower in healthy volunteers than in patients with septic shock (p < .0001) between days 1 and 3 after onset of the septic shock and not significantly different between nonsurvivor and survivor patients (p = .1278). However, median S100A9 messenger RNA measured on days 7-10 was significantly higher in patients who were about to contract hospital-acquired infections compared with those who were not (p = .009). In the multivariate analysis, the S100A9 marker increased the probability of contracting hospital-acquired infections with an odds ratio of 1.12 per unit (p = .0054).

S100A9 messenger RNA is increased in septic shock and its delayed overexpression is associated with the occurrence of secondary hospital-acquired infection. This biomarker may be of major interest in identifying patients with increased risk of hospital-acquired infection who could benefit from targeted therapy aimed at restoring their immune functions.