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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.
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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.
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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).
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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.
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5.
Acute, food-induced moderate elevation of plasma uric acid protects against hyperoxia-induced oxidative stress and increase in arterial stiffness in healthy humans.
Vukovic, J, Modun, D, Budimir, D, Sutlovic, D, Salamunic, I, Zaja, I, Boban, M
Atherosclerosis. 2009;(1):255-60
Abstract
We examined the effects of acute, food-induced moderate increase of plasma uric acid (UA) on arterial stiffness and markers of oxidative damage in plasma in healthy males exposed to 100% normobaric oxygen. Acute elevation of plasma UA was induced by consumption of red wine, combination of ethanol and glycerol, or fructose. By using these beverages we were able to separate the effects of UA, wine polyphenols and ethanol. Water was used as a control beverage. Ten males randomly consumed test beverages in a cross-over design over the period of 4 weeks, one beverage per week. They breathed 100% O(2) between 60(th) and 90(th)min of the 4-h study protocol. Pulse wave augmentation index (AIx) at brachial and radial arteries, plasma antioxidant capacity (AOC), thiobarbituric acid-reactive substances (TBARS), lipid hydroperoxides (LOOH) assessed by xylenol orange method, UA and blood ethanol concentrations were determined before and 60, 90, 120, 150 and 240 min after beverage consumption. Consumption of the beverages did not affect the AIx, TBARS or LOOH values during 60 min before exposure to hyperoxia, while AOC and plasma UA increased except in the water group. Significant increase of AIx, plasma TBARS and LOOH, which occurred during 30 min of hyperoxia in the water group, was largely prevented in the groups that consumed red wine, glycerol+ethanol or fructose. In contrast to chronic hyperuricemia, generally considered as a risk factor for cardiovascular diseases and metabolic syndrome, acute increase of UA acts protectively against hyperoxia-induced oxidative stress and related increase of arterial stiffness in large peripheral arteries.
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6.
[Effect of ethanol on metabolic syndrome].
Jelski, W, Szmitkowski, M
Polskie Archiwum Medycyny Wewnetrznej. 2007;(7):306-11
Abstract
Metabolic syndrome is characterized by a group of risk factors for cardiovascular diseases, such as abdominal obesity, low high-density lipoprotein (HDL) cholesterol, elevated triglycerides, elevated arterial blood pressure, insulin resistance or impaired glucose tolerance. A number of studies focused on the relationship between alcohol consumption and prevalence of metabolic syndrome and its individual components. Ethanol can either aggravate the syndrome or prevent it--this depends primarily on the amounts and types of alcohol beverages consumed. It is commonly believed that moderate alcohol consumption is associated with a decreased incidence of metabolic syndrome and beneficial effects on plasma lipid levels, waist circumference and fasting plasma glucose. Of all the components of metabolic syndrome, the most beneficial effect of ethanol arises from an increase in plasma HDL cholesterol levels. The relationship between alcohol consumption and incidence of metabolic syndrome is more pronounced among red wine drinkers because polyphenoles contained in red wine increase the activity of endothelial nitric oxide synthase (eNOS), which plays a key role in the pathogenesis of metabolic syndrome. Decreased activity of this enzyme contributes to the development of insulin resistance, arterial hypertension and dyslipidemia. Stimulation of eNOS activity, which participates in the transport of HDL molecules, may provide an explanation for the mechanism of the increase in plasma levels of this particular lipid fraction in response to ethanol. Endothelial nitric oxide synthase requires the presence of antioxidants, which prevent both inactivation of nitric oxide in the reaction with peroxide anions and the accumulation of peroxynitrates.
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7.
[Alcohol-induced gastrointestinal diseases].
Szalay, F
Orvosi hetilap. 2003;(34):1659-66
Abstract
UNLABELLED Alcohol induced gastrointestinal diseases are common and significant, and may lead to early death. The annual death caused by alcoholic liver disease and pancreatitis in Hungary is up to 8000. Metabolites, mainly acetaldehyde and free radicals are responsible for the injury. Although the alcohol itself is not carcinogenic, some maligancies are more common among alcoholics. AIM AND METHODS In this review the hepatic and extrahepatic metabolism of alcohol, the epidemiology, pathomechanism, clinical signs of the alcohol induced organ damages and the treatment options are summarized. RESULTS Type IV alcoholdehydrogenase in the stomach has a role in the first pass metabolism. The liver is the main place of the metabolism. If the amount of alcohol exceeds the metabolising capacity, the toxic substances cause lipidperoxidation, membrane and organ injury. Alcohol metabolism is different in the pancreas, the activity of fatty acid ethanol ester synthase activity is more pronounced. In alcoholics the leukoplakia, oropharingeal carcinoma, oesophagitis, Mallory-Weiss syndrome, liver cirrhosis related oesophageal variceal bleeding, chronic gastritis, liver diseases, pancreatitis, bowel motility disorders, malabsorption and colorectal carcinoma are more frequent. The fatty liver remains reversible for a long. Following steatohepatitis, fibrosis, cirrhosis and liver carcinoma may develop. Despite growing knowledge of the role of endotoxins, cytokines, nutritional, immunological and genetic factors, it is still unknown why the given disease will develop in a patient, and there is no parameter for determining the point of irreversibility of the alterations. The possibilities for medical treatment are limited, since some patients do not cooperate properly, and on the other hand, the drugs and measurements can control only a part of the whole process (antioxidants, anti-inflammatory drugs, monoclonal anti-cytokine antibodies), and are appropriate only for the treatment of complications as ascites, portal hypertension, oesophageal varices, portosystemic encephalopathy, malabsortion, infections, vitamin deficiency. CONCLUSIONS Therefore the prevention and abstinence are very important. The task of the general practitioner and the role of the cooperation among the patient, the physician, the family and the community are very important.
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8.
Preoperative nutritional support at home in head and neck cancer patients: from nutritional benefits to the prevention of the alcohol withdrawal syndrome.
Bertrand, PC, Piquet, MA, Bordier, I, Monnier, P, Roulet, M
Current opinion in clinical nutrition and metabolic care. 2002;(4):435-40
Abstract
PURPOSE OF REVIEW Preoperative nutritional support in severely malnourished patients decreases complications after major surgery. This review summarizes previous studies on head and neck cancer patients undergoing surgery, and offers recommendations on preoperative nutritional support based on the literature and our experience. RECENT FINDINGS Head and neck cancer has a large impact on the patient's quality of life and a high mortality rate. Aggressive surgical resection followed by soft-tissue and osseous reconstruction is the gold standard of treatment. The incidence of postoperative complications is high at 20-50%. Malnutrition and alcohol withdrawal syndrome are often present, and are considered risk factors for developing wound infection after head and neck cancer surgery. Proactive intervention by preoperative nutritional support may correct nutrient deficiencies, minimize malnutrition-related morbidity and mortality, reduce the length and cost of hospitalization, and may prevent alcohol withdrawal syndrome. Nutritional support given preoperatively for 7-10 days decreases postoperative complications by approximately 10% in malnourished patients with weight loss of 10% or more. Oral liquid supplements and enteral nutrition are useful to support head and neck cancer patients preoperatively. Enteral nutrition is safer, more physiological, less expensive and practicable at home compared with parenteral nutrition, which is not usually indicated in these patients. SUMMARY Enteral nutrition is efficient in preoperative phase to prevent postoperative complications. However evidence is insufficient to conclude that preoperative immune-enhancing enteral feeding provides any supplementary benefit by comparison with a standard diet. Our experience with the preoperative approach in head and neck cancer patients is reported in this paper.