1.
Zinc deficiency as a mediator of toxic effects of alcohol abuse.
Skalny, AV, Skalnaya, MG, Grabeklis, AR, Skalnaya, AA, Tinkov, AA
European journal of nutrition. 2018;(7):2313-2322
Abstract
OBJECTIVE To review data on the role of ethanol-induced alteration of Zn homeostasis in mediation of adverse effects of alcohol abuse. METHODS The scholarly published articles on the association between Zn metabolism and alcohol-associated disorders (liver, brain, lung, gut dysfunction, and fetal alcohol syndrome) have been reviewed. RESULTS It is demonstrated that alcohol-induced modulation of zinc transporters results in decreased Zn levels in lungs, liver, gut, and brain. Zn deficiency in the gut results in increased gut permeability, ultimately leading to endotoxemia and systemic inflammation. Similarly, Zn deficiency in lung epithelia and alveolar macrophages decreases lung barrier function resulting in respiratory distress syndrome. In turn, increased endotoxemia significantly contributes to proinflammatory state in alcoholic liver disease. Finally, impaired gut and liver functions may play a significant role in alcoholic brain damage, being associated with both increased proinflammatory signaling and accumulation of neurotoxic metabolites. It is also hypothesized that ethanol-induced Zn deficiency may interfere with neurotransmission. Similar changes may take place in the fetus as a result of impaired placental zinc transfer, maternal zinc deficiency, or maternal Zn sequestration, resulting in fetal alcoholic syndrome. Therefore, alcoholic Zn deficiency not only mediates the adverse effects of ethanol exposure, but also provides an additional link between different alcohol-induced disorders. CONCLUSIONS Generally, current findings suggest that assessment of Zn status could be used as a diagnostic marker of metabolic disturbances in alcohol abuse, whereas modulation of Zn metabolism may be a potential tool in the treatment of alcohol-associated disorders.
2.
Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity: how poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease.
Fernandes, LMP, Bezerra, FR, Monteiro, MC, Silva, ML, de Oliveira, FR, Lima, RR, Fontes-Júnior, EA, Maia, CSF
European journal of clinical nutrition. 2017;(5):580-586
Abstract
Ethanol is an important risk factor for the occurrence of several brain disorders that depend on the amount, period and frequency of its consumption. Chronic use of ethanol often leads to the development of neurodegenerative syndromes, which cause morphological and functional impairments such as foetal alcohol syndrome in newborns exposed to ethanol during pregnancy, Wernicke-Korsakoff Syndrome and, more rarely, Marchiafava-Bignami disease (MBD). MBD is characterized by primary degeneration of the corpus callosum, without inflammation and is associated with oxidative stress and hypovitaminosis, as well as altered mental status, to mention dementia, seizures, depression and so on. This review discusses MBD and poor nutrition as a risk factor for the development of such alcoholic syndrome, with focus on diagnosis, pathogenic aspects, signs and symptoms, as well as therapeutic perspectives. On the basis of the inclusion/exclusion criteria adopted, the performed search in scientific databases (Pubmed, Scielo and Google Scholar) resulted in 100 studies that are being presented and discussed in the present work. Review, case-control and cohort studies on alcoholism-associated hypovitaminosis, oxidative stress, MBD and ethanol metabolism pathways were admitted as relevant. We highlight that MBD is a poorly described, diagnosed, insidious and progressive condition, for which evidence suggests a synergism between ethanol-induced neurotoxic effects and hypovitaminosis B. Present treatment consists of vitamin B1(thiamine) supplementation. Nonetheless, other strategies such as the inclusion of antidepressants or steroidal anti-inflammatories as add-on therapies have been employed as an attempt to improve the damage. Indeed, both the diagnosis and treatment are difficult, and death occurs within few years.
3.
Auto-brewery syndrome: Ethanol pseudo-toxicity in diabetic and hepatic patients.
Hafez, EM, Hamad, MA, Fouad, M, Abdel-Lateff, A
Human & experimental toxicology. 2017;(5):445-450
Abstract
Endogenous alcohol has been applied for spontaneous ethanol production via different metabolic pathways of the human body. Auto-brewery syndrome describes the patients with alcohol intoxication after ingesting carbohydrate-rich meals. The main objective of this study is to investigate the effect of diabetes mellitus (DM), liver cirrhosis (LC) and presence of both (DM and LC) on blood alcohol concentration (BAC) especially after carbohydrate ingestion. BAC has been measured by headspace gas chromatography-mass spectrometry in three groups of humans namely control, DM, LC and both (DM and LC) groups. The results showed that BAC in control group was 0.01-.3 mg/dL with mean 0.3 ± 0.41 mg/dL. In patients with DM, BAC is significantly higher than that of control group 4.85 ± 3.96 mg/dL. In patients with LC, BAC was 3.45 ± 2.65 mg/dL. In patients with both DM and LC, BAC increases to reach 10.88 ± 5.36 mg/dL. Endogenous ethanol production appears to increase in DM and LC. Also, it increased much more in patients with both diseases, but it did not reach toxic levels. On comparing BAC and blood glucose level in each group, all groups show insignificant correlations ( p > 0.05).
4.
[The efficacy of remaxol addition in the treatment of alcohol withdrawal syndrome].
Vinnikova, MA, Utkin, SI, Nenasteva, AY, Zakharov, MV
Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova. 2016;(1):40-46
Abstract
OBJECTIVE To study the efficacy of remaxol addition in the treatment scheme of alcohol withdrawal syndrome. MATERIAL AND METHODS Eighty patients with alcohol dependence and physical symptoms of alcohol withdrawal syndrome were enrolled. All patients received basic therapy in accordance to the applicable standards of treatment. The patients were randomized to remaxol introduced intravenously 2 times a day (morning and afternoon) in dose of 400 ml for 7 days (n=40) and saline with 25%-magnesium sulfate (10 ml) and 4% potassium chloride (10 ml) (n=40). RESULTS The effectiveness of the inclusion of remaxol was expressed in a more rapid relief of asthenic syndrome, reduction of phenomena such as tension, dysphoria, headache and impaired coordination of samples. Patients treated with remaxol demonstrated a trend towards a more rapid reduction of the affective (p=0.08) and behavioral components (p=0.09) of the syndrome of pathological craving for alcohol. Hepatoprotective and detoxification properties of the drug were confirmed by the significant decline in ALT and AST activity to the 20th day of treatment. Significant positive changes in lipid metabolism (HDL to the 7th day of treatment) and a normalizing effect on the processes of tissue respiration were shown as well. No adverse effects were noted. CONCLUSION The data obtained allow to recommend the inclusion of remaxol in the complex treatment regimens of alcohol withdrawal syndrome to improve the treatment efficacy.