title: Evidence for intestinal and liver epithelial cell injury in the early phase of sepsis.
abstract: The development of sepsis and multiple organ failure are important determinants of the outcome in critically ill patients. Hepatosplanchnic hypoperfusion and resulting intestinal and hepatic cell damage have been implicated as central events in the development of sepsis and multiple organ failure. Our aim was to study (1) the relation between intramucosal perfusion and intestinal and hepatic cell damage in an early phase of sepsis and (2) the correlation of these parameters with mortality. Two groups of patients were consecutively selected after intensive care unit admission: patients with postoperative abdominal sepsis (n = 19) and patients with pneumonia-induced sepsis (n = 9). Intramucosal perfusion was assessed by gastric tonometry (Pr-aCO2 gap, Pico2). Circulating levels of intestinal fatty acid binding protein (I-FABP) and liver (L)-FABP were used as markers for intestinal and hepatic cellular damage, respectively. Outcome was determined on day 28. Pr-aCO2 gap correlated with I-FABP (Pearson r = 0.56; P < 0.001) in all patients, and gastric mucosal Pico2 correlated significantly with I-FABP (r = 0.57; P = 0.001) in patients with abdominal sepsis. At intensive care unit admission, nonsurvivors had significantly higher I-FABP and L-FABP values than survivors (I-FABP: 325 vs. 76 pg/mL, P < 0.04; L-FABP: 104 vs. 31 ng/mL, P < 0.04). Patients with abdominal sepsis was especially responsible for high-admission I-FABP and L-FABP levels in nonsurvivors (I-FABP: 405 vs. 85 pg/mL, P < 0.04; L-FABP: 121 vs. 59 ng/mL, P < 0.04). This study shows that splanchnic hypoperfusion correlates with intestinal mucosal damage, and that elevated plasma levels of I-FABP and L-FABP are associated with a poor outcome in critically ill patients with abdominal sepsis.
authors.affiliation: Department of Surgery, University Hospital Maastricht & Nutrition and Toxicology Research Institute (NUTRIM), Maastricht University, Maastricht, The Netherlands.
authors.forename: Joep P M
authors.initials: JP
authors.lastname: Derikx
authors.forename: Martijn
authors.initials: M
authors.lastname: Poeze
authors.forename: Annemarie A
authors.initials: AA
authors.lastname: van Bijnen
authors.forename: Wim A
authors.initials: WA
authors.lastname: Buurman
authors.forename: Erik
authors.initials: E
authors.lastname: Heineman
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D016638:Critical Illness; D004847:Epithelial Cells / Q000378:metabolism; D050556:Fatty Acid-Binding Proteins / Q000097:blood*; D005260:Female; D006801:Humans; D007022:Hypotension / Q000097:blood / Q000401:mortality / Q000503:physiopathology; D007413:Intestinal Mucosa / Q000098:blood supply / Q000293:injuries* / Q000378:metabolism / Q000503:physiopathology; D007422:Intestines / Q000098:blood supply / Q000293:injuries* / Q000503:physiopathology; D008099:Liver / Q000098:blood supply / Q000293:injuries* / Q000378:metabolism / Q000503:physiopathology; D008102:Liver Circulation; D008297:Male; D008365:Manometry; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood* / Q000209:etiology / Q000401:mortality / Q000503:physiopathology; D010477:Perfusion; D011014:Pneumonia / Q000097:blood / Q000150:complications / Q000503:physiopathology; D018805:Sepsis / Q000097:blood* / Q000209:etiology / Q000401:mortality / Q000469:parasitology; D013997:Time Factors
chemical_list: D015415:Biomarkers; D050556:Fatty Acid-Binding Proteins