Intramucosal pH and endotoxin and cytokine release in severe acute pancreatitis

It has been postulated that in severely ill patients splanchnic hypoperfusi on may cause endotoxin release from the gut, and this leakage of endotoxin into the circulation can trigger the cascade of inflammatory cytokines. We tested this hypothesis in 9 patients with acute severe pancreatitis by moni toring gastric intramucosal pH (pHi) as measure of splanchnic hypoperfusion at 12-h intervals trying to correlate it to endotoxin and cytokine release . Only 3 of 59 samples, obtained from 3 patients contained circulating endo toxin. Thirteen of 15 plasma samples drawn at pHi <7.20 did not contain end otoxin. The pHi was significantly lower in patients who subsequently develo ped 3 or more organ failures (P = 0.0017, analysis of variance). Although e ndotoxemia was only occasionally found, most patients had measurable interl eukin 1 beta (IL-1 beta), interleukin 6 (IL-6), interleukin 8 (IL-8), and i nterleukin 10 (IL-10) in their plasma. Concentrations of IL-6, IL-8, and IL -10 on admission correlated to degree of organ dysfunction as measured by t he multiple organ system failure score (P = 0.035, r = 0.74; P = 0.010, r = 0.91; P = 0.021, r = 0.82, respectively). In conclusion, patients with acu te, severe pancreatitis often have splanchnic hypoperfusion and produce a w ide array of cytokines despite a rare occurrence of endotoxemia.