Implication of interleukin 18 and intercellular adhesion molecule (ICAM)-1 in acute pancreatitis

Irrespective of the underlying etiology the immune response to is almost identical in severe cases of acute pancreatitis. While the triggering factors of acute pancreatitis are still poorly understood, cytokines are considered as important mediators in the pathophysiology of severe acute pancreatitis. However, only few studies have investigated the role of IL-18 and ICAM-1 in human acute pancreatitis.

Levels of IL-18 and sICAM-1 were studied in 87 patients with acute pancreatitis. Samples were obtained immediately on admission, thereafter on the third, seventh, fourteenth and twenty-first day after admission. Ascites or peripancreatic exudate was obtained by ultrasound-guided fine needle aspiration in 19 patients at the day of admission.

Necrotizing pancreatitis was associated with significantly elevated levels of IL-18 and sICAM-1. Concentrations of IL-18 decreased after the first week of the disease in patients with non-complicated course, whereas levels remained high in patients with persistent multiple organ dysfunction syndrome (MODS) and infection of necrosis. Peak levels of sICAM-1 were observed at the time of admission with a subsequent decrease during the observation period. These mediators showed clear correlations with the disease severity, development of MODS, and infected necrosis.

These proinflammatory mediators seem to be involved in the pathogenesis of severe acute pancreatitis, correlate with the disease severity and may be applied as prognostic markers.