Intestinal hypoperfusion contributes to gut barrier failure in severe XXXX .

@entity1 @entity844 @entity5694 @entity788 @entity656 @entity63 @entity33 @entity177 @entity1630 @entity158 @entity968 @entity1851
@entity177 and subsequent bacterial translocation have been implicated in the development of organ dysfunction and septic complications associated with severe @entity656 . Splanchnic hypoperfusion and @entity63 /reperfusion injury have been postulated as a cause of increased intestinal permeability. The urinary concentration of intestinal @entity844 binding protein ( @entity1630 ) has been shown to be a sensitive marker of @entity63 , with increased levels being associated with @entity63 /reperfusion. The aim of the current study was to assess the relationship between excretion of @entity1630 in urine, gut @entity33 (intestinal hyperpermeability and systemic exposure to @entity5694 ), and clinical severity. @entity1 with a clinical and biochemical diagnosis of @entity656 were studied within 72 hours of onset of @entity158 . @entity968 probes of 3350 kDa and 400 kDa were administered enterally, and the ratio of the percentage of retrieval of each probe after renal excretion was used as a measure of intestinal macromolecular permeability. Collected urine was also used to determine the @entity1630 concentration ( @entity1630 -c) and total @entity1630 ( @entity1630 ) excreted over the 24-hour period, using an enzyme-linked immunosorbent assay technique. The systemic inflammatory response was estimated from peak 0 to 72-hour plasma @entity1851 levels, and systemic exposure to endotoxins was measured using serum IgM endotoxin cytoplasmic antibody (EndoCAb) levels. The severity of the attack was assessed on the basis of the Atlanta criteria. Sixty-one @entity1 with @entity656 (severe in 19) and 12 healthy control subjects were studied. Compared to mild attacks, severe attacks were associated with significantly higher urinary @entity1630 -c (median 1092 pg/ml vs. 84 pg/ml; P < 0.001) and @entity1630 (median 1.14 microg vs. 0.21 microg; P = 0.003). Furthermore, the control group had significantly lower @entity1630 -c (median 37 pg/ml; P = 0.029) and @entity1630 (median 0.06 microg; P = 0.005) than @entity1 with mild attacks. @entity1630 correlated positively with the @entity968 3350 percentage retrieval (r = 0.50; P < 0.001), CRP (r = 0.51; P < 0.001), and inversely with serum IgM EndoCAb levels (r = -0.32; P = 0.02). The results of this study support the hypothesis that splanchnic hypoperfusion contributes to the loss of intestinal mucosal integrity associated with a severe attack of @entity788 .
