The role of IL17-A in the second hit of acute pancreatitis

Abstract

Background: Acute pancreatitis is characterised by distinct clinical phases. An initial systemic inflammation response syndrome (SIRS) and occasional subsequent ‘second hit’ usually initiated by systemic sepsis. The pro-inflammatory T-helper 17 pathway has been shown to be an initiator of early SIRS in AP, however to date interleukin-17A has not been evaluated as a marker of the septic second hit in SAP. Methods: Seventeen patients (aged 28-65) with mild (n=10), moderate (n=1) and severe (n=6) acute pancreatitis were enrolled. Peripheral blood samples were drawn on days 7, 9, 11 and 13 of illness for routine clinical markers as well as cytokine analysis. Flow cytometry was performed using a Th1/Th2/Th17 Cytokine Bead Array (BD Biosciences). Statistical analysis was performed using a Mann-Whitney U tests, with a p=value of <0.05 considered significant. Results: The mean concentration of IL-17A on days 7, 9, 11 and 13 in mild and severe acute pancreatitis patients were 2.45, 2.11, 2.12, 6.91 and 3.63, 3.48, 5.76, 3.56 pg/ml respectively, with no statistical significance between the two groups. Statistically significant differences exist between the mild and severe acute pancreatitis groups regarding the mean WCC (7.38 & 23.49), CRP (73.6 & 245.3) and PCT (0.37 & 20.7). Conclusion: The IL-17A concentration in the study population did not statistically identify the second hit of acute pancreatitis. Further studies to confirm this are underway.