title: Early gut barrier dysfunction in patients with severe acute pancreatitis: attenuated by continuous blood purification treatment.
abstract: OBJECTIVE
  The aim of this study was to investigate the effect of continuous blood purification (CBP) on early gut mucosal dysfunction in patients with severe acute pancreatitis (SAP).
  
  
  METHODS
  Patients with SAP were randomized to receive 24 hours of continuous veno-venous hemofiltration (CVVH; n = 33) or no CVVH (n = 30). Blood samples were taken from the patients at 0, 6, 12, and 24 hours during CVVH therapy. Serum diamine oxidase (DAO) and endotoxin, epithelial permeability, transepithelial electrical resistance (TER) and F-actin rearrangement of the epithelial monolayer were used as the markers for the assessment of gut barrier function and the effect of CBP therapy in patients with SAP.
  
  
  RESULTS
  Patients with SAP had increased levels of serum DAO, endotoxin, and epithelial permeability when compared with normal controls, and the increase was more pronounced in patients with organ dysfunction (p<0.01). F-actin rearrangement, loose cell-cell junction, and iNOS mRNA upregulation were found in all patients. After CBP treatment, Acute Physiology and Chronic Health Evaluation II score and SOFA score improved significantly; levels of serum DAO, endotoxin, and epithelial permeability decreased(p<0.05). CBP also significantly attenuated reorganization of actin and downregulated iNOS mRNA expression and NO production (p<0.05).
  
  
  CONCLUSIONS
  CBP can not only improve the general conditions but also effectively improve gut barrier dysfunction. The beneficial effect of CBP on gut barrier dysfunction is associated with the improvement of cytoskeletal instability, by downregulating iNOS through the removal of excess proinflammatory factors.
authors.affiliation: Department of Nephrology Diseases, The Third Affiliated Hospital of Nanchang University, Nanchang, JiangXi, China. zjb7526@163.com
authors.forename: Jianbin
authors.initials: J
authors.lastname: Zhang
authors.forename: Chen
authors.initials: C
authors.lastname: Yuan
authors.forename: Gan
authors.initials: G
authors.lastname: Hua
authors.forename: Ruyan
authors.initials: R
authors.lastname: Tong
authors.forename: Xiangfeng
authors.initials: X
authors.lastname: Luo
authors.forename: Zhou
authors.initials: Z
authors.lastname: Ying
mesh_terms: D018806:APACHE; D000199:Actins / Q000378:metabolism; D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D006631:Amine Oxidase (Copper-Containing) / Q000097:blood; D015415:Biomarkers / Q000097:blood; D018938:Caco-2 Cells; D002681:China; D017097:Electric Impedance; D004731:Endotoxins / Q000097:blood; D005260:Female; D006440:Hemofiltration; D006801:Humans; D007365:Intercellular Junctions / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D010195:Pancreatitis / Q000097:blood / Q000150:complications / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D010539:Permeability; D012333:RNA, Messenger / Q000378:metabolism; D012720:Severity of Illness Index; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D013997:Time Factors; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D000199:Actins; D015415:Biomarkers; D004731:Endotoxins; D012333:RNA, Messenger; D009569:Nitric Oxide; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D006631:Amine Oxidase (Copper-Containing)