Artikel
Alcohol consumption damages the intestinal barrier and increases systemic LPS bioactivity in healthy volunteers – facts that might aggravate outcome in intoxicated trauma patients
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Veröffentlicht: | 22. Oktober 2019 |
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Gliederung
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Objectives: Trauma is the leading cause of death of young adults and alcohol consumption is a major cause of accidents. Severely injured patients frequently develop an immunological imbalance in the aftermath of a trauma, which often results in infectious complications, sepsis and multi organ failure. In this context alcohol plays a crucial role. Intestinal small fatty acid binding proteins (I-FABP) are localized intracellularly or in the plasma membrane of enterocytes of the small intestine. Damage to the intestinal barrier results in a release of I-FABP into the extracellular space. Similarly, soluble CD14 (sCD14) serves as an indirect marker for LPS translocation. Here, we measured both markers in a time-dependent manner after acute alcohol consumption.
Methods: 20 healthy volunteers consumed an individually calculated amount of alcohol every 20 minutes for a period of four hours, which resulted in a blood alcohol level of 1.0 pro mille. Peripheral whole blood was taken before drinking (time, t0) as control and every two hours after the start of alcohol drinking over the following six hours, after 24 and 48 hours, respectively. LPS Bioactivity and enterocyte damage were assessed by measuring sCD14 and I-FABP levels in serum with ELISA.
Results and conclusion: The intestinal FABP in serum is significantly reduced two hours after the onset of alcohol consumption and remained decreased after four hours. However, six hours after beginning, I-FABP was significantly elevated compared to previous measurements as well as to normal values (p<0,05). This alteration remains even after 24 hours. No significant differences were found after 48 hours compared to t0. Soluble CD14 in serum remained close to the normal values during the first hours after onset of alcohol consumption, but was significantly elevated after 24 and 48 hours (p<0,05).
Our data demonstrate that even moderate amounts of alcohol damage the intestinal barrier in healthy volunteers, and that this damage persists for days. Furthermore, the increased levels of soluble CD14 indicate an enhanced systemic LPS bioactivity, which is caused by increased intestinal permeability for pathogens. This fact should be considered in trauma patients with acute alcohol intoxication, since those patients may have an increased risk for post-traumatic infections. This is the focus of our future clinical studies.