Circulating endotoxin, tumour necrosis factor-alpha, and their natural antagonists in the pathophysiology of acute pancreatitis.

Inflammatory mediators, such as endotoxin and tumour necrosis factor-alpha (TNF-alpha) have been implicated in the pathogenesis of acute pancreatitis. However, serum levels of these mediators in patients with acute pancreatitis are often not detectable on hospital admission. In contrast, their circulating antagonists (antiendotoxin antibodies and soluble TNF-alpha receptors) are detectable in all patients. With increasing severity of disease, patients are more likely to manifest a fall in antiendotoxin levels, suggesting exposure to endotoxin. Similarly, there is a stepwise increase in soluble TNF-alpha receptors with increasing severity of disease. This suggests that the degree of TNF-alpha-induced inflammation correlates with disease severity. The role of endotoxin, TNF-alpha and their relevant antagonists as markers or mediators of the systemic complications of acute pancreatitis remains under investigation.