The Enteral Factor in Pancreatic Infection

Foitzik, T.

doi:10.1159/000055814

Cited by 15 publications

(7 citation statements)

References 46 publications

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“…Bacterial translocation is related to mucosal damage caused by hemodynamic and microvascular dysfunction, intravascular thrombosis, vasodilatation, hypotension, and endothelial damage triggered by TNF‐α [28]. Our present data show high and similar levels of TNF‐α in both groups that underwent induction of AP.…”

Section: Discussionsupporting

confidence: 66%

Effect of inhibition of prostaglandin E2 production on pancreatic infection in experimental acute pancreatitis

Matheus

Coelho

Sampietre

et al. 2007

HPB

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Section: Discussionsupporting

confidence: 66%

Effect of inhibition of prostaglandin E2 production on pancreatic infection in experimental acute pancreatitis

Matheus

Coelho

Sampietre

et al. 2007

HPB

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“…Recent reviews on intestinal barrier dysfunction in acute pancreatitis have focused on bacterial translocation and the intestinal origin of sepsis [5, 6]. However, this paper will explore how the intestine, as both culprit and victim, influences the pathophysiology of SAP (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

The role of the intestine in the pathophysiology and management of severe acute pancreatitis

Flint

Windsor

2003

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BackgroundThe outcome of severe acute pancreatitis has scarcely improved in 10 years. Further impact will require new paradigms in pathophysiology and treatment. There is accumulating evidence to support the concept that the intestine has a key role in the pathophysiology of severe acute pancreatitis which goes beyond the notion of secondary pancreatic infection. Intestinal ischaemia and reperfusion and barrier failure are implicated in the development of multiple organ failure. DiscussionConventional management of severe acute pancreatitis has tended to ignore the intestine. More recent attempts to rectify this problem have included 1) resuscitation aimed at restoring intestinal blood¯ow through the use of appropriate¯uids and splanchnic-sparing vasoconstrictors or inotropes; 2) enteral nutrition to help maintain the integrity of the intestinal barrier;3) selective gut decontamination and prophylactic antibiotics to reduce bacterial translocation and secondary infection.Novel therapies are being developed to limit intestinal injury, and these include antioxidants and anti-cytokine agents. This paper focuses on the role of the intestine in the pathogenesis of severe acute pancreatitis and reviews the implications for management.

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“…Pancreatic infection has been identified as the main determinant of morbidity and mortality in SAP [31] . Necrotic pancreatic tissue represents an ideal environment for bacterial replication and pancreatic infection which can fuel SIRS and increase the mortality rate [30,32] . The occurrence of infection in other tissues such as liver, lymph node, and blood is less frequent in AP as demonstrated in a previous study from our laboratory [18] .…”

Section: Discussionmentioning

confidence: 99%

Do the Effects of Pentoxifylline on the Inflammatory Process and Pancreatic Infection Justify Its Use in Acute Pancreatitis?

et al. 2009

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The Enteral Factor in Pancreatic Infection

Cited by 15 publications

References 46 publications

Effect of inhibition of prostaglandin E2 production on pancreatic infection in experimental acute pancreatitis

Effect of inhibition of prostaglandin E2 production on pancreatic infection in experimental acute pancreatitis

The role of the intestine in the pathophysiology and management of severe acute pancreatitis

Do the Effects of Pentoxifylline on the Inflammatory Process and Pancreatic Infection Justify Its Use in Acute Pancreatitis?

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