Intestinal permeability and systemic endotoxemia in patients with acute pancreatitis

The bacterial contamination of pancreatic necrosis in acute pancreatitis is supposed to occur through translocation of intestinal bacteria. The aim of this clinical study was to evaluate intestinal mucosa permeability and endotoxemia in patients with acute pancreatitis.

Sixtythree patients with acute pancreatitis were studied. Classification 42 patients had mild and 21 patients severe pancreatitis. Intestinal permeability was assessed at day 0, 1, 3, 7, 9 and 11 using the lactulose/mannitol differential absorption test. Serial venous blood samples were taken at 0, 30, 60, 90, 120, and 180 minutes, at 12, 24 hours, and at days 3, 7, 9 and 11 for endotoxin measurement

Patients with severe pancreatitis had higher intestinal barrier dysfunction compared with patients with mild pancreatitis, the L:M ratio being 0.36 ± 0.15 and 0.051 ± 0.013 respectively (p< 0.05). The systemic endotoxin concentration were higher in patients with severe pancreatitis as regards mild pancreatitis (p < 0.05). A significant correlation was observed between the maximum systemic endotoxin concentration and intestinal permeability measured at day 7 in patients with mild (rs = 0.721; p = 0.001) and severe (rs = 0.956; p= 0.001) pancreatitis.

Gut permeability is increased in patients with acute pancreatitis. Patients with severe pancreatitis may be more exposed to impaired gut barrier function. Moreover the pancreatits (especially severe) can lead to systemic endotoxemia. This agrees with the hypothesis that the splanchnic hypoperfusion, during the pancreatitis, may impair intestinal mucosal barrier function and contribute to the systemic inflammatory response and multiorgan failure.

Acute pacreatitis, Endotoxemia, Intestinal permeability.