Plasmid labeling confirms bacterial translocation in pancreatitis

Wang

J. Zhejiang Univ. - Sci. B

2007

Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis (SAP) in multiple organ injury is a hotspot in the surgical field. In clinical practice, the main complicated organ dysfunctions are shock, respiratory failure, renal failure, encephalopathy, with the rate of hepatic diseases being closely next to them. The hepatic injury caused by SAP cannot only aggravate the state of pancreatitis, but also develop into hepatic failure and cause patient death. Its complicated pathogenic mechanism is an obstacle in clinical treatment. Among many pathogenic factors, the changes of vasoactive substances, participation of inflammatory mediators as well as OFR (oxygen free radical), endotoxin, etc. may play important roles in its progression.

Section: Role Of Endotoxinmentioning

confidence: 99%

Study progress on mechanism of severe acute pancreatitis complicated with hepatic injury

Wang

J. Zhejiang Univ. - Sci. B

2007

“…Experimental studies indicated that pancreatic infection in SAP appeared to be due to translocation of bacteria from the gut to mesenteric lymph nodes, peritoneal fluid and blood, then from these sites to the pancreas itself. Several experimental studies revealed that acute pancreatitis (AP) promotes bacterial translocation, which in turn leads to infection of the pancreas and septic complications (Foitzik et al, 1994;Kazantsev et al, 1994). The main mechanisms that governed the processes of bacterial translocation in SAP are probably related to the over-growth of enteric flora due to intestinal dysfunction, damage to intestinal permeability and impairment of host immunity (Foitzik et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Effect of Lactobacillus plantarum enteral feeding on the gut permeability and septic complications in the patients with acute pancreatitis

et al. 2007

Eur J Clin Nutr

Objective: To study the effect of the Lactobacillus plantarum (LP) enteral feeding on the gut permeability and sepsis in the patients with acute pancreatitis. Subjects: Seventy-six subjects who stayed over 1 week in the hospital completed the study. Subjects were not treated with any lactobacillus supplement before the intervention. Methods: Seventy-six patients with acute pancreatitis were randomly divided into two groups, parenteral nutrition (PN) group (n ¼ 38) and ecoimmunonutrition (EIN) group supplied by LP enteral feeding (n ¼ 36). The acute physiology and chronic health evaluation score, Balthazar CT score, CRP, fecal bacterial species and DNA fingerprint profiles as well as the potentially pathologenic organisms in nasogastric aspirate were determined on the day of admission and on the 8 day. The intestinal permeability was assessed by measurement of the ratio of lactulose/rhamnose on the day of admission and on days 5 and 8. The rate of organ failure, septic complications and death cases were evaluated at the 8 day. Results: Following 7 days treatment, 38.9% patients in the EIN group were colonized with multiple organisms compared to 73.7% in the PN group (Po0.01), and 30.6% patients in the EIN grew potentially pathogenic organisms compared to 50% patients in PN group (Po0.05). The fecal bacterial DNA fingerprint profiles were less, the amount of lactobacteria and bifydobacteria decreased, and the amount of enterococci increased in PN group as compared with EIN group, Po0.05. By day 8, the lactulose/rhamnose ratio in EIN group were lower than that in PN group at days 5 and 8, Po0.05. The patients with LP got a better clinical outcomes as compared with the patients with PN. Conclusion: EIN enteral feeding can attenuate disease severity, improve the intestinal permeability and clinical outcomes.

“…Meanwhile, the process will further increase intestinal permeability and promote continuous invasion of intestinal bacteria and endotoxin into body to form an infernal circle. Moreover, when intestinal permeability has been increased to certain levels, some macromolecule substances, such as bacteria and lipopolysaccharide, can penetrate the injured intestinal mucosa to move towards multiple organs and lead to a secondary infection of pancreatic tissue (de las Heras et al, 2000;Kazantsev et al, 1994;Gloor et al, 2001;Schwarz et al, 2000), which is the main cause of deaths of AP patients (Carnovale et al, 2005;Furuya et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

J. Zhejiang Univ. - Sci. B

Song

et al. 2007

Acute pancreatitis (AP) is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition.AP can cause an injury of intestinal mucosa barrier, leading to translocation of bacteria or endotoxin through multiple routes, bacterial translocation (BT), gutorigin endotoxaemia, and secondary infection of pancreatic tissue, and then cause systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), which are important factors influencing AP's severity and mortality. Meanwhile, the injury of intestinal mucosa barrier plays a key role in AP's process. Therefore, it is clinically important to study the relationship between the injury of intestinal mucosa barrier and AP. In addition, many factors such as microcirculation disturbance, ischemical reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier. In this review, we summarize studies on mechanisms of AP.