2008
DOI: 10.1097/mpa.0b013e31815a399f
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Early Gut Mucosal Dysfunction in Patients With Acute Pancreatitis

Abstract: Intestinal mucosal function is injured in early phase of AP especially in patients with organ dysfunction, which may be a stimulus for development of multiple organ dysfunction and correlate with bad outcome in AP patients.

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Cited by 103 publications
(88 citation statements)
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“…Increased intestinal permeability was confirmed by several methods in patients with acute pancreatitis [77,78,79,80]. The intestinal permeability was correlated with plasma endotoxin [77,79,80], serum TNF-α [77,80], IL-6, CRP, and the severity index estimated by computed tomography [80].…”
Section: Acute Pancreatitismentioning
confidence: 99%
See 1 more Smart Citation
“…Increased intestinal permeability was confirmed by several methods in patients with acute pancreatitis [77,78,79,80]. The intestinal permeability was correlated with plasma endotoxin [77,79,80], serum TNF-α [77,80], IL-6, CRP, and the severity index estimated by computed tomography [80].…”
Section: Acute Pancreatitismentioning
confidence: 99%
“…The intestinal permeability was correlated with plasma endotoxin [77,79,80], serum TNF-α [77,80], IL-6, CRP, and the severity index estimated by computed tomography [80]. The urinary concentration of intestinal fatty acid-binding protein, a sensitive marker of intestinal ischemia, correlated positively with intestinal permeability, which suggests that splanchnic hypoperfusion induces the loss of intestinal mucosal integrity [78].…”
Section: Acute Pancreatitismentioning
confidence: 99%
“…Possible relationship between psoriasis and pancreatitis remains an enigma. A noteworthy hypothesis could be that of intestinal barrier dysfunction, all the more since some authors reported increased intestinal permeability in patients with acute pancreatitis [44,45]. There is, however, another possibility.…”
Section: Discussionmentioning
confidence: 93%
“…Researchers have found that inflammatory mediators contribute to early SAP causing systemic epithelial barrier dysfunction [22] and increased vascular endothelial permeability [23]. The gut fuels SAP [24], which activates development of a local or systemic inflammation response and secondary infection of pancreatic necrosis [22,25].…”
Section: Discussionmentioning
confidence: 99%