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To assess nutritional risk of alcoholic patients admitted for alcohol detoxification.Screening of nutritional risk of alcoholic patients using the Malnutrition Universal Screening Tool.Fifty-three percentage patients at presentation were rated as being at medium or high risk of malnutrition.Malnutrition should be actively considered and screened for in alcoholic patients admitted for alcohol detoxification due to its high prevalence and benefits obtained from treatment.

Ethanol exerts its behavioural effects largely by interacting with receptors for brain neurotransmitters. However, the molecular mechanisms involving these interactions and the pathogenesis of alcohol-withdrawal symptomatology are still not well understood. Until recently, no data were available about homocysteine (Hcy) levels in acute alcohol intoxication of chronic alcoholics and in patients undergoing withdrawal from alcohol. Hcy, blood-alcohol concentrations, vitamins B6, B12, and folate concentrations were assessed in 29 chronic alcoholics, who underwent withdrawal from alcohol. We observed increased Hcy levels in most patients. Hcy levels steadily decreased during the observation period. We postulate that hyperhomocysteinaemia and excitatory amino acid neurotransmitters, by their agonism at the N-methyl-D-aspartate receptor, may partly mediate alcohol-associated withdrawal symptomatology. The importance of assessing serum Hcy levels in order to detect methylation deficiency in patients with chronic alcoholism and for possible therapeutic strategies is discussed.

The present study investigated the effect of acute intragastric (i.g.) administration of dry Hypericum perforatum extract (HPE), containing 0.3% hypericin, on ethanol intake in genetically selected Marchigian Sardinian alcohol-preferring (msP) rats. The i.g. administration of HPE, 125 or 250 mg/kg, induced a 30-40% reduction in ethanol intake in rats offered 10% (v/v) ethanol for 2 h/day. The effect of these doses was selective, since they modified neither food intake nor food-associated drinking; neither did the same doses modify the rat's gross behaviour in the open-field test. A dose of 500 mg/kg frequently induced immobility and a general suppression of ingestive behaviour. In rats offered 10% ethanol for 12 h/day, ethanol intake following treatment with 250 mg/kg HPE was significantly lower than that of controls for up to 10 h. The effect on ethanol intake was not related to the antidepressant-like effect of HPE revealed in the forced swimming test. In this regard, the effect on ethanol intake was observed after a single administration of 125 mg/kg, whereas the antidepressant effect was observed only after repeated treatment with doses higher than 125 mg/kg HPE. The i.g. administration of HPE, 250 mg/kg, did not affect blood-alcohol levels following i.g. treatment with 0.7 g/kg ethanol, the amount usually ingested in a single drinking episode; thus, the effect is not related to changes in the pharmacokinetics of ethanol. The present study shows that HPE markedly reduces ethanol intake in msP rats, without significantly modifying food intake.

Coma and vomiting are the commonest symptoms in young teenagers intoxicated by alcohol. Severe toxicity, manifested as coma, occurs at lower blood alcohol concentrations in young teenagers than in adults. The effect of ethanol on the state of consciousness is directly proportional to blood alcohol concentration. Among children under 5 years of age the risk of hypoglycaemia is increased. A significant risk in acute alcohol intoxication is the rapid development of coma, which in cold environments could lead to fatal hypothermia. Preschool-age children are reported to eliminate ethanol twice as fast as adults, whereas young teenagers eliminate it at the adult rate. The biochemical disturbances in children 11 to 16 years of age with alcohol intoxication resemble those of adults. Mild acidosis of a respiratory or metabolic origin and mild hypokalaemia are common findings in young teenagers. Fluid replacement with glucose-containing fluids and follow-up are generally the only treatments needed for complete recovery. Motives leading to alcohol intoxication are a wish to get drunk, experimenting, problems in human relations, and attempted suicide. The underlying problems are often family-related, such as divorce, an alcoholic parent and a lower socioeconomic group.

Abstract Aims Minimum unit price (MUP) of 50 pence per unit of alcohol was introduced in Scotland on the 1 May 2018. We assessed alcohol-related liver disease (ArLD) discharges from Glasgow Royal Infirmary (GRI) before and after the introduction of MUP. Methods Medical records of all patients discharged from Gastroenterology wards at GRI in the fourth quarter (Q4) of the years 2015–2019 were reviewed. All patients with ArLD were identified, and detailed hospitalization data were collected retrospectively. Active drinking, severity scores, presence of alcoholic hepatitis (AH) and 90-day mortality and readmission rates were assessed. Results There were fewer ArLD discharges per quarter after MUP than before (mean 80.3 pre-MUP; mean 68 post-MUP), and the proportion of active drinkers was lower post-MUP (64.7 vs. 70.5%). There was a significant fall in the mean number of weekly discharges of individual patients who were actively drinking (4.0 ± 2.0 pre-MUP, 2.8 ± 1.5 post-MUP, P = 0.01). There were no differences in the proportion of patients presenting with ascites, encephalopathy or AH; however, there was a reduction in presentations with acute upper gastrointestinal bleeding from 15.8% pre-MUP to 7.4% post-MUP (P = 0.02; odds ratio 0.42). Severity of liver disease remained unchanged. The 90-day mortality and readmission rates were not significantly different. Conclusion Since the introduction of MUP there has been a reduction in the absolute numbers of patients discharged with ArLD and the number of individual patients involved at GRI. The pattern of clinical presentation was largely unaffected with overall ArLD severity, readmission rates and 90-day mortality similar pre- and post-MUP.

Abstract Aims The UK government aims to develop alcohol care teams (ACTs) that provide care for alcohol dependence in general hospital settings. Service descriptors have been identified to support the development of ACTs. The aim of this study was to use Delphi panel principles to identify the clinical competencies required to provide these elements of service. Methods We formed an expert consensus panel of 24 senior clinical alcohol practitioners, leaders and experts by experience drawn from all regions of England. The study was divided into three distinct phases: (a) a review and synthesis of current literature in this area, (b) a face-to-face meeting of the expert panel and (c) subsequent iterations to refine the competencies until consensus was reached. Results Our initial search strategy resulted in 555 competency statements being extracted from a range of national clinical professional and occupational standards and other sources. The research team refined these statements to 98 competencies in advance of the expert meeting. The panel identified 14 additional statements and reduced the number of competencies to 78. Subsequent iterations finalized 72 competencies across the 8 service descriptors. Conclusions Drawing on the existing published resources and clinical experience, the expert panel has provided consensus on the core clinical competencies required for alcohol care teams in caring for hospitalized patients with alcohol use disorders. Whilst it is acknowledged that the range of current provision is variable, these competencies provide a template for clinical practice and the development of multidisciplinary ACTs.

The heptic metabolism of acetaldehyde in carbon tetrachloride (CCl4)-intoxicated rats was studied using a non-recirculating haemoglobin-free liver-perfusion system. Acetaldehyde uptake by the liver from acutely CCl4-treated animals (4.16 mmol/kg,i.p.) at 24 hr after the treatment was not significantly altered, whereas that by the liver from chronically CCl4-treated animals (2.08 mmol/kg,i.p., twice a week, for 8-12 weeks) was decreased by approximately 50% when it was determined in the presence of 0.01-5 mM acetaldehyde. In liver from rats chronically intoxicated with CCl4, the following important biochemical changes were observed: (1) The activity of low Km aldehyde dehydrogenase (ALDH) in hepatic mitochondria was decreased by approximately 75%. (2) The basal levels of the lactate/pyruvate (cytosolic [NADH]/[NAD+]) ratio as well as the beta-hydroxybutyrate/acetoacetate (mitochondrial [NADH]/[NAD+]) ratio were elevated by more than 2-fold. (3) Mitochondrial NADH oxidation was also reduced by approximately 35% of the control level. (4) The basal level of hepatic oxygen uptake was attenuated by approximately 50%, and the infusion of acetaldehyde (0.01-5.0 mM) caused a further decrease in the uptake. (5) The rate of ethanol production from acetaldehyde by the catalytic action of alcohol dehydrogenase was found to be unaltered when low concentrations of acetaldehyde (0.01-0.2 mM) were used, whereas a significant suppression of the rate of ethanol production was detected in the presence of high concentrations of acetaldehyde (0.6-5 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

We have studied the effect of acute administration of ethanol when it replaced morphine in step-down passive avoidance task on the test day and the effects of antagonists of GABAergic, opioidergic and cholinergic systems on ethanol actions.Morphine (5 mg/kg, s.c.) was administered as pre-training and 24 h later as pre-test drug, and the latencies were measured in mice. Ethanol (0.125, 0.25, 1 and 2 g/kg, i.p.) was administered instead of pre-test morphine. Antagonists of GABAergic (bicuculline 0.5, 1 and 2 mg/kg, i.p.), opioidergic (naloxone 0.06, 0.25 and 1 mg/kg, i.p.) and cholinergic (atropine 0.625 and 1.25 mg/kg, i.p. and mecamylamine 0.5, 1 and 2 mg/kg, i.p.) systems were co-administered with ethanol (0.25 g/kg, i.p.) on the test day. Locomotor activity was measured as well.Pre-training morphine impaired the memory on the test day which was restored when the same dose of morphine was used as pre-test drug. All four doses of ethanol replaced pre-test morphine and enhanced the memory. This effect was prevented by all of the above antagonists. No significant changes were seen in the locomotor activity of the animals treated with ethanol or antagonists compared to the proper controls.GABAergic, endogenous opioidergic and cholinergic systems are involved in the memory recall improvement by ethanol when it replaced morphine on the test day. A review of the literature suggests other possibilities such as the release of intermediate neurotransmitters.