PubMed · 13959471
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S FREEMAN. 1963. The drinking driver.. https://pubmed.ncbi.nlm.nih.gov/13959471/
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The high frequency of excessive drinking among populations of western countries justifies screening strategies by primary health care givers. The intervention following the identification of a problem drinker should be adjusted according to the nature and level of alcohol-related risk or harm. A non-judgmental and benevolent dialogue about alcohol consumption is to be carried out with every patient, for in most cases this is enough to identify anyone concerned by at-risk or harmful drinking and to assess any consequences and dependence levels. Standardized questionnaires have been conceived and validated to encourage practitioners to carry out this type of interview, taking into account two contradictory needs: a systematic approach of the screening and the need for rapidity. In the same objective, among all sorts of "brief interventions" the efficient ones have been adapted to target populations and to be acceptable to the clinicians' point of view. These tools have been conceived to help excessive drinkers reduce their alcohol consumptions, but they can be a model for a more general approach to secondary prevention, considering all risk factors, not only hazardous behaviour to health.
Recent findings from our laboratory have shown that acute alcohol (EtOH) intoxication before burn injury impairs intestinal immunity and barrier functions. To further delineate the mechanism of impaired intestinal barrier function, the present study examined the role of corticosterone (CORT) and interleukin (IL)-18, as CORT and IL-18 are elevated following a combined insult of EtOH intoxication and burn injury. Male rats (approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL prior to burn or sham injury (25% total body surface area). Immediately after injury, a group of rats was treated with CORT synthesis inhibitor metyrapone (25 mg/kg), with or without recombinant (r)IL-18 (50 microg/kg). Another group of rats was treated with caspase-1 inhibitor Ac-YVAD-CHO to block IL-18 production. On Day 1 after injury, there was a significant increase in blood CORT levels, intestinal levels of IL-18, neutrophil chemokines [cytokine-induced neutrophil chemoattractant 1 (CINC-1) and CINC-3], intercellular adhesion molecule-1, myeloperoxidase activity, and intestinal permeability in rats receiving a combined insult of EtOH and burn injury. Treatment of rats with CORT inhibitor or with caspase-1 inhibitor prevented the increase in all of the above parameters following a combined insult of EtOH and burn injury. Moreover, coadministration of rIL-18 in metyrapone-treated rats restored the above parameters, similar to those observed in rats receiving EtOH and burn injury. These findings suggest that a combined insult of EtOH and burn injury results in increased CORT levels, which in turn up-regulates intestinal IL-18 levels and thereby causes altered intestinal barrier function following a combined insult of EtOH intoxication and burn injury.
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