The Correlation Between Endotoxemia And Small Intestinal Bacterial Overgrowth In Acute Pancreatitic Patients

Acute pancreatitis is a kind of inflammation owning to the activation ofpancreatic enzyme in pancreas resulting from many causes, which leads toautodigestion, edema, hemorrhage and necrosis of pancreas. Acute pancreatitisis a clinical common acute abdomen and is divided into mild acute pancreatitisand severe acute pancreatitis. There is a urgent onset, rapid progress andhigher mortality up to30%in severe acute pancreatitis. The intestinal barrierfunction plays a key role in the pathogenesis of acute pancreatitis. Intestinaltract is the nuclear and initiating organ leading to multiple organ dysfunction.Bacterial translocation and enterogenous endotoxemia following to impairedintestinal barrier function may lead to infection and excessive activation ofwhite blood cells and macrophages, which release a large number ofinflammatory factors such as interleukin1, interleukin10, interleukin8, tumornecrosis factor alpha, etc. These inflammatory factors act as a second-hit to thebody, which can lead to systemic inflammatory response syndrome andmultiple organ dysfunction.Small intestinal bacterial overgrowth is a very heterogeneous syndromecharacterised by an increased number and/or abnormal type of bacteria in thesmall bowel. Most authors consider diagnostic of small intestinal bacterialovergrowth to be the finding of≥105bacteria [i.e. colony-forming units(CFU)] per ml of proximal jejunal aspiration. The normal value is≤104CFU/ml. Now lactulose or glucose hydrogen breath test is most commonlyused for the clinical diagnose of small intestinal bacterial overgrowth.Endotoxin namely lipopolysaccharide is a Gram-negative bacterial cellwall component and consists of three structural domains including lipid A, anoligosaccharide core and the distal O-antigen. It is discharged after thebacterial death. Live bacteria can also release of endotoxin in the form of vesication. Endotoxin is a potent stimulus for the neutrophils and macrophagesto chemotaxis, mobile and release reaction. The activatied neutrophils andmacrophages with the stimulation of endotoxin release a large number ofinflammatory cytokines, leading to the damage to cells and tissues, clinicallycharacterized by SIRS and impaired viscera function.Interleukin8as part of the CXC chemokines, mainly produced bymononuclear macrophages, endothelial cells, etc, is capable of the neutrophilschemotaxis and can induce the degranulation of the neutrophils to releaseelastase, lysosomal enzyme, oxygen free radical, leading to local and systemicinflammatory response. Interleukin8can activate and direct the white bloodcells to inflammation and induce the neutrophils to release various enzymesand a large number of oxygen free radicals, resulting in the injury of pancreasand systemic organs in acute pancreatitis.Objectives: This study intends to investigate the relationship ofendotoxin, interleukin8and small intestinal bacteria growth in patients withacute pancreatitis through the monitoring of serum endotoxin, interleukin8inacute pancreatitic patients and lactulose hydrogen breath test to detect if smallintestinal bacteria growth is existed in acute pancreatitic patients and provide anew way for the treatment of acute pancreatitis.Methods: Acute pancreatitic patients were divided into mild acutepancreatitis group and severe acute pancreatitis group according to theChinese guide of acute pancreatitis management (2003). Fifteen healthyvolunteers were taken as control group. The blood samples were got fromacute pancreatitic patients in the morning on an empty stomach on the first,third and seventh day after admission for the determination of serumendotoxin and interleukin8.On the first day all the patients had a lactulosehydrogen breath test. The healthy volunteers had a lactulose hydrogen breathtest in the morning on an empty stomach on the same day on which their bloodsamples were got for the determination of serum endotoxin and interleukin8.Results:①The serum endotoxin on the first day and third day in MAPwere higher than the control group (P<0.05). The serum endotoxin on the seventh day in MAP was not statistically significant comparing with thecontrol group (P>0.05). The serum endotoxin on the first day, third day andseventh day in SAP were higher comparing with the MAP (P<0.05). Theserum endotoxin on the first day, third day and seventh day in MAP and SAPdecreased progressively (P<0.05);②The serum interleukin8on the first day,third day and seventh day in MAP were higher than the control group(P<0.05). The serum interleukin8on the first day, third day and seventh dayin SAP were higher comparing with the MAP (P<0.05). The serum interleukin8on the first day, third day and seventh day in MAP and SAP decreasedprogressively (P<0.05);③Nobody had a positive lactulose hydrogen breathtest for SIBO in the control group. Three patients had a positive lactulosehydrogen breath test for SIBO in MAP on the first day with a rate of12%.Seven patients had a positive lactulose hydrogen breath test for SIBO in SAPon the first day with a rate of46.7%. The rate of SIBO in SAP was higher thanthe MAP (P<0.05);④We had a correlation analysis between SIBO and serumendotoxin level on the first day and found that SIBO and serum endotoxinlevel were correlative. The contingency coefficient was0.463. The serumendotoxin of SIBO group in both MAP and SAP were higher than withoutSIBO group (P<0.05);⑤We had a correlation analysis between SIBO andserum interleukin8level on the first day and found that SIBO and seruminterleukin8level were correlative. The contingency coefficient was0.450.The serum interleukin8of SIBO group in both MAP and SAP were higherthan without SIBO group (P<0.05);⑥We had a correlation analysis betweenserum endotoxin level and serum interleukin8level on the first day and foundthat serum endotoxin had a positive correlation with interleukin8(rs0.984).Conclusions:1Endotoxemia was existed in acute pancreatitic patients during the earlystage and serum endotoxin can be an indicator for the severity assessmentand the prognosis in acute pancreatitis.2There was small intestinal bacterial overgrowth in acute pancreatiticpatients. The occurrence of small intestinal bacterial overgrowth was associated with the severity of acute pancreatitis.3Endotoxemia and small intestinal bacterial overgrowth were correlativeand the occurrence of endotoxemia may be associated with small intestinalbacterial overgrowth in acute pancreatitic patients.4Interleukin8was involved in the inflammatory response in acute pancrea-titis and can be used as an auxiliary index of the severity assessment inacute pancreatitis. Small intestine bacterial overgrowth may be involved inthe inflammatory response in acute pancreatitis through the endotoxinwhich promoted the release of interleukin8.