Markers of intestinal injury are associated with endotoxemia in successfully resuscitated patients

High Level of Endotoxemia Following Out-of-Hospital Cardiac Arrest Is Associated With Severity and Duration of Postcardiac Arrest Shock*

“…However, considering the complex pathophysiology of post-CA shock, the contribution of endotoxemia to shock severity remains unknown. In a preliminary study, we found that biomarkers of intestinal injury were altered after CA and were associated with endotoxemia, suggesting that endotoxemia results from gut translocation (9). In the present study, we hypothesized that endotoxemia could contribute to the severity of post-CA shock.…”

Induced Hypothermia Preserves the Functional Enterocyte Mass in A Porcine Multiple Trauma Model

“…Therefore Piton et alÕs definition, which was developed from work with a mixed critically ill patient cohort, might not be applicable in this posttraumatic setting. Previously, iFABP has been described as increasing early after trauma (13) and as normalising rapidly between day two and three after admission (29). Therefore the increase of iFABP in TH might be due to a reduced metabolism with a prolonged increase under hypothermic conditions (20).…”

“…In particular, the microvascular mucosal oxygenation appears to be improved after severe traumatic insults (22,28). However, Besides plasma citrulline as a marker for the functional enterocyte mass, iFABP has been described as a valid marker for enterocyte necrosis following shock (8,9,15,29). In contrast to the expected decrease of plasma citrulline, iFABP did not increase significantly in TN.…”

The Gut Microbiome and the Brain

“…27 In addition, visceral pain sensitivity thresholds are reduced and visceral pain (provoked by rectal distension) is rated as more unpleasant after administration of low-dose LPS. 28 Increased exposure to gut microbiome-derived LPS (endotoxemia) may occur in the elderly, in whom it is diminished by yogurt consumption, 29 as a consequence of small intestinal bacterial overgrowth (SIBO), 30,31 and secondary to increased intestinal permeability resulting from extreme physiologic stress, 32 ethanol exposure, 33 or a ''fast-food style'' Western diet, high in both carbohydrate and saturated fat. 34 LeClercq et al 35 have reported increased intestinal permeability, elevated blood LPS and peptidoglycan levels, and low-grade systemic inflammation associated with psychological symptoms of alcohol dependence in alcohol-dependent subjects.…”