Immunological changes of mild acute pancreatitis in late-stage alcoholic chronic pancreatitis.

The exact immunological mechanisms underlying alcoholic chronic pancreatitis are unclear. To investigate the role of the tumor necrosis factor (TNF) receptor pathway the serum levels of TNF-alpha, soluble TNF receptors -p55/-p75, and CRP were determined by ELISA in 34 patients with late-stage alcoholic chronic pancreatitis and 28 controls. The disease activity (Balthazar scoring system) of acute pancreatitis on the background of late-stage chronic pancreatitis correlated with an increase of functionally active TNF receptor -p55/-p75 serum levels. Unstimulated peripheral blood mononuclear cells are one source of soluble TNF receptors and demonstrated a systemic leukocyte activation. The marked enhancement of soluble TNF receptors suggests that alcoholic chronic pancreatitis may be characterized by transient peaks of in situ TNF-alpha production preceding a long-lasting release of soluble TNF receptors. The data demonstrate immunological changes characteristic of acute pancreatitis in late-stage alcoholic chronic pancreatitis.