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Статті в журналах з теми "Chronic Alcohol Abuse"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

Andersson, Sture, Erja Halmesmäki, Martti Koivusalo, Risto Lapatto, and Olavi Ylikorkala. "Placental Alcohol Metabolism in Chronic Alcohol Abuse." Neonatology 56, no. 2 (1989): 90–93. http://dx.doi.org/10.1159/000243107.

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2

Büttner, Andreas. "Neuropathology of Chronic Alcohol Abuse." Academic Forensic Pathology 4, no. 2 (June 2014): 180–87. http://dx.doi.org/10.23907/2014.029.

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3

Caradoc-Davies, Gillian. "Feigned Alcohol Abuse." British Journal of Psychiatry 152, no. 3 (March 1988): 418–20. http://dx.doi.org/10.1192/bjp.152.3.418.

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A man presenting with factitious alcohol abuse and its alleged complications is described. It is argued that chronic factitious disorders are more logically viewed as part of that spectrum of conditions where there is abnormal illness behaviour, including somatoform disorders and other related conditions, than as separate nosological or diagnostic entities.

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4

Maleki, Nasim, and Marlene Oscar-Berman. "Chronic Pain in Relation to Depressive Disorders and Alcohol Abuse." Brain Sciences 10, no. 11 (November 7, 2020): 826. http://dx.doi.org/10.3390/brainsci10110826.

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Chronic pain disorders have been associated separately with neuropsychiatric conditions such as depression and alcohol abuse. However, in individuals who suffer from non-cancer chronic pain disorders, it is not clear if the burden of depressive disorders is similar for those with and without a history of alcohol abuse. Using data from the Collaborative Psychiatric Epidemiology Surveys (CPES), we found depressive disorders to have a high burden in men and women with a history of alcohol abuse, independently of the presence or absence of chronic pain. We also found that, although the incidence of persistent depressive disorder was comparable in men and women with a history of alcohol abuse, and significantly higher than in control men and women, the incidence of a major depressive episode was higher in women with a history of alcohol abuse independently of the presence or absence of chronic pain. The age of onset of depressive disorders, independently of pain status, was younger for individuals with a history of alcohol abuse. The findings of this study have important implications for the clinical management of individuals who suffer from chronic pain comorbidly with depression and/or alcohol abuse.

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5

Levine, Harris, and Morgan. "Energy expenditure in chronic alcohol abuse." European Journal of Clinical Investigation 30, no. 9 (September 2000): 779–86. http://dx.doi.org/10.1046/j.1365-2362.2000.00708.x.

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6

Bechtler, M., D. Schilling, and J. F. Riemann. "Chronic alcohol abuse and increasing dysphagia." DMW - Deutsche Medizinische Wochenschrift 130, no. 27 (July 2005): 1641–42. http://dx.doi.org/10.1055/s-2005-871883.

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7

Nguyen, Tom, M. Mazen Jamal, and Timothy R. Morgan. "Alcohol abuse and chronic hepatitis C." Current Hepatitis Reports 6, no. 3 (August 2007): 119–24. http://dx.doi.org/10.1007/s11901-007-0014-7.

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8

Fernandez Miranda, J. J., D. F. Frías Ortiz, F. C. Maria Francina, P. Rossi, and O. W. Muquebil Ali Al Shaban Rodríguez. "Alcoholic hallucinosis after chronic alcohol abuse: A case report." European Psychiatry 41, S1 (April 2017): s861—s862. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1721.

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IntroductionAlcoholic hallucinosis is a rare complication of chronic alcohol abuse and a prevalence of 0.6–0.7% in alcoholics has been reported.Case reportA 54-year-old Indian immigrant in Barcelona was referred for psychiatric evaluation in April 2016 by due of his behavioral alterations. Evaluation revealed that he was apparently asymptomatic when he come to Spain, 18 years ago. He had been consuming alcohol since 1974 and gradually the frequency and quantity increased to 600 mL of rum daily by 1996. He complained of hearing voices of family members, being irritable even when he was alone and in catatonic phases. He was found to be gloomy, reclusive, not sleeping and talking to oneself. He used to have sleep disturbances; irritability and tremors when temporarily stopped alcohol consumption. He presented a clinical abstinence syndrome, with pharmacological resistance to benzodiazepine perfusion: it was necessary to use dexmedetomidine an Alpha2-agonist with sedative and analgesic properties. After 12 days of medical treatment on UCI, he recovered from abstinence syndrome and was transferred to psychiatry ward. Blood analysis showed raised aspartate amino transferase and alanine amino transferase. Computed tomography and magnetic resonance imaging brain revealed bilateral lateral ventricle enlargement with narrowing of lower end of Aqueduct of Sylvius. He was treated with oral paliperidone. The dose was gradually increased to 18 mg/day and he responded quickly. In the follow-up, he was abstinent from alcohol, compliant with treatment and free from all kinds of hallucinations after medication adherence and psychotherapy.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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9

Peycheva, K., and E. Boteva. "Effect of Alcohol to Oral Health." Acta Medica Bulgarica 43, no. 1 (March 1, 2016): 71–77. http://dx.doi.org/10.1515/amb-2016-0009.

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SummaryAccording to the World Health Organization there are almost two billion people worldwide who consume alcohol on a regular basis. It’s a common abuse and almost 80 million are diagnozed with “alcohol abuse disorders” (WHO 2002, 2004). Excessive alcohol consumption is related to more than 60 different medical conditions, as suicide, homicide and different forms of accidents. Some conditions are acute, while other conditions such as liver cirrhosis, chronic pancreatitis, haemorrhagic stroke and various forms of cancer, are chronic consequences. Non-carious destructions of teeth like dental erosion are also associated with frequent alcohol consumption, because of precipitation of salivary proline-rich proteins caused by polyphenols present in most alcoholic drinks. The high concentration of organic and inorganic acids and the habit of keeping the alcoholic drink in the mouth can cause chronic inflammations of the soft tissues in the mouth and can increase the negative side effects from metals of crowns, bridges, orthodontic devises and various restorations. A literature review has been made due to the authors clinical observations and experiences.

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10

Lee, Dong Hun, Jong Sung Lee, Il Ho Lee, and Jin Tae Hong. "Therapeutic potency of fermented field water-dropwort (Oenanthe javanica (Blume) DC.) in ethanol-induced liver injury." RSC Advances 10, no. 3 (2020): 1544–51. http://dx.doi.org/10.1039/c9ra08976d.

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11

Ragan, Paul W., Charles K. Singleton, and Peter R. Martin. "Brain Injury Associated With Chronic Alcoholism." CNS Spectrums 4, no. 1 (January 1999): 66–68. http://dx.doi.org/10.1017/s1092852900011226.

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AbstractAlcoholism can result in a number of severe consequences to the central nervous system, including Korsakoff's psychosis, delusions, delirium, Wernicke's encephalopathy, and cerebellar degeneration. Many of these disorders have a substantially higher prevalence than had been previously believed. Neuropathologic and neuroimaging studies have been instrumental in identifying the changes undergone by the alcoholic brain and the factors that may contribute to alcohol-induced brain damage. Biologic differences appear to make women especially susceptible to central nervous system insult from alcohol abuse. The damage caused by alcohol may be associated, in part, with thiamine deficiency, neuronal excitotoxicity, and magnesium wasting.

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12

Kick, Steven D. "Evaluation and Management of Chronic Alcohol Abuse." Hospital Practice 34, no. 4 (April 15, 1999): 95–106. http://dx.doi.org/10.3810/hp.1999.04.137.

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13

Brown, Lou Ann S., Robert T. Cook, Thomas R. Jerrells, Jay K. Kolls, Laura E. Nagy, Gyongyi Szabo, Jack R. Wands, and Elizabeth J. Kovacs. "Acute and Chronic Alcohol Abuse Modulate Immunity." Alcoholism: Clinical and Experimental Research 30, no. 9 (September 2006): 1624–31. http://dx.doi.org/10.1111/j.1530-0277.2006.00195.x.

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14

Bailes, Barbara K. "Chronic alcohol abuse in elderly surgical patients." AORN Journal 65, no. 5 (May 1997): 963–71. http://dx.doi.org/10.1016/s0001-2092(06)62979-7.

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15

Arapostathi, C., N. Tentolouris, and E. B. Jude. "Charcot foot associated with chronic alcohol abuse." Case Reports 2013, apr05 1 (April 5, 2013): bcr2012008263. http://dx.doi.org/10.1136/bcr-2012-008263.

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16

Appenzeller, Brice M. R., Serge Schneider, Michel Yegles, Armand Maul, and Robert Wennig. "Drugs and chronic alcohol abuse in drivers." Forensic Science International 155, no. 2-3 (December 2005): 83–90. http://dx.doi.org/10.1016/j.forsciint.2004.07.023.

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17

Ingraham, Kirby, Steven Kaplan, and Fong Chan. "Rehabilitation Counselors' Awareness of Client Alcohol Abuse Patterns." Journal of Applied Rehabilitation Counseling 23, no. 3 (September 1, 1992): 18–22. http://dx.doi.org/10.1891/0047-2220.23.3.18.

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In this article, we examined the extent of alcohol abuse among several groups of individuals with other disabilities. We then compared our results with rehabilitation counselors estimates of alcohol abuse in the same client groups. One hundred and thirty-four rehabilitation clients were administered the Michigan Alcoholism Screening Test (MAST) at the time of initial interview to determine their level of alcohol consumption and/or abuse. The results indicated that clients with chronic mental illness and those with limitations resulting from physical trauma have a appreciably higher rate of alcohol abuse than the other identified client groups (those with congenital & developmental disabilities) or the general population. When we asked 40 rehabilitation counselors to estimate probable alcohol abuse rates for these client groups, we found that the counselors slightlyoverestimated alcohol abuse problems among people with congenital and development disabilities, and appreciably underestimated the prevalence of alcohol abuse among clients with physically induced trauma or chronic mentallllness. The results suggest that rehabilitation counselors may lack awareness about this “hidden disability,” within selected client groups, and, the results also imply a need for improved counselor training related to alcohol abuse issues in rehabilitation populations.

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18

Schwan, Raymund. "Lorazepam reduced recurrent alcohol-related seizures in chronic alcohol abuse." ACP Journal Club 131, no. 3 (November 1, 1999): 63. http://dx.doi.org/10.7326/acpjc-1999-131-3-063.

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19

Labib, M., M. Abdel-Kader, L. Ranganath, S. Martin, and V. Marks. "Impaired Renal Tubular Function in Chronic Alcoholics." Journal of the Royal Society of Medicine 82, no. 3 (March 1989): 139–41. http://dx.doi.org/10.1177/014107688908200307.

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Despite the well known effects of chronic alcohol abuse on the gastrointestinal, cardiovascular, nervous and endocrine systems, little information is available on its effect on renal function. To assess renal function we measured urinary excretion of albumin, α1 microglobulin and retinol binding protein in 30 chronic alcoholic patients. Our data shows that 40% of chronic alcoholic patients have impaired renal tubular function.

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20

S.P Girish and Jagan Mohan B. Reddy. "Associated Liver Disease in Alcoholic Chronic Pancreatitis." Academia Journal of Surgery 3, no. 1 (July 5, 2020): 172–75. http://dx.doi.org/10.47008/ajs/2020.3.1.37.

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Background: Alcohol is a common etiological factor in the pathogenesis of both pancreatic and liver disease. The frequencies of associated liver histological change in patients with alcoholic chronic pancreatitis (AICP) vary from series to series. Significant proportion of patients with alcoholic pancreatitis does have histological changes in liver. Subjects and Methods: The study was conducted at Narayana Medical College & Hospital, Chintareddy Palem, Nellore, Andhra Pradesh on liver-biopsy specimens from 23 patients with chronic alcoholic pancreatitis subjected to operation for pain, from August 2015 to July 2016 and all the patients had undergone liver biopsy at the time of surgery for AICP. The patients were followed as part of a prospective study of 33 patients who had been treated for chronic pancreatitis. The pathologists were requested to report on alcohol related histological changes in the specimen. Results: There were 23 patients and all were men. Chronic pancreatitis was due to alcohol abuse in all patients. The median age at surgery was 39.8 years. The mean duration of alcohol abuse was 20.5 years (range 6-29 years).The average alcohol intake was 122gm 36gms/day. Three patients had jaundice for 3-6 months duration. None of the patients had any other risk factor for liver disease and none of them had clinical or biochemical evidence of liver disease. The histological reports were, 4 patients had alcoholic hepatitis, 2 severe steatohepatitis, 1 granulomatous hepatitis, 3 cholestasitc changes, one fatty liver and 12 had no significant pathology. None of the patients had cirrhosis. Thus significant alcoholic liver disease was present in 30.4% (7/23) of the patients. There was no increased incidence of post-operative mortality and morbidity in patients with liver pathology. Conclusion: As reported in many other series, chronic alcoholic pancreatitis is associated with histological changes in liver in significant proportion of patients. However its clinical significance and prognosis of these patients are unknown.

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21

Moskowitz, Ralph M., and Anthony J. Errichetti. "Cardiovascular Evaluation After Withdrawal from Chronic Alcohol or Cocaine-Alcohol Abuse." Journal of Addictive Diseases 10, no. 4 (October 5, 1991): 47–65. http://dx.doi.org/10.1300/j069v10n04_04.

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22

Dudek, Iga, Danuta Hajduga, Cezary Sieńko, Amr Maani, Elżbieta Sitarz, Monika Sitarz, and Alicja Forma. "Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options." Current Pathobiology Reports 8, no. 4 (October 23, 2020): 87–97. http://dx.doi.org/10.1007/s40139-020-00214-w.

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Abstract Purpose of the Review Alcohol abuse causes a wide range of disorders that affect the nervous system. These include confusion, cerebellar ataxia, peripheral neuropathy, and cognitive impairment. Chronic and excessive alcohol consumption is the primary cause of peripheral neuropathy. It is worth noting that peripheral neuropathy has no reliable treatment due to the poor understanding of its pathology. Recent Findings Coasting is a major feature of alcoholic neuropathy, largely due to chronic alcohol abuse. Its major features are hyperalgesia, allodynia, and burning pain. Even though much research was done in this area, still we do not have a full understanding of the mechanism of alcoholic neuropathy. However, some theories have been proposed. These include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis also seem to be implicated in the pathophysiology of this alcoholic neuropathy. The goal of treatment is to impede further damage to the peripheral nerves while also restoring their normal physiology. Alcohol abstinence, intake of balanced diets, and treatment with medications are suggested including benfotiamine, alpha-lipoic acid, acetyl-l-carnitine, vitamin E, methylcobalamin, myo-inositol, N-acetylcysteine, capsaicin, tricyclic antidepressants, or antiepileptic drugs. Summary This review focuses on the many pathways that play a role in the onset and development of alcohol-induced neuropathy, as well as present the possible treatment strategies of this disorder, providing insights into a further search of new treatment modalities.

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23

Tsarev, Sergei A., Andrei V. Shcherban, Sergei A. Suslin, Aleksei A. Katin, and Il'ya I. Sirotko. "ADVANCED APPROACH TO DIAGNOSTICS OF CHRONIC ALCOHOL ABUSE." Science and Innovations in Medicine 4, no. 1 (March 15, 2019): 37–41. http://dx.doi.org/10.35693/2500-1388-2019-4-1-37-41.

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Objectives - to identify the criteria of selecting the applicants for professional drivers who require the carbohydrate-deficient transferrin (CDT) assay, which can be applied by an addiction psychiatrist. Material and methods. The extensive analysis of testing results of 232 patients admitted to Samara Regional Narcological Dispensary from its local subsidiaries in Samara and the Samara Region was carried out. Results. The fact of driving in drunk condition in the past was defined as the criterion having the diagnostic value. Conclusion. The patients with the known fact of drunk driving had the majority of positive test results of the chronic alcohol abuse, compared to other groups of patients in this study. These findings make it possible to declare the deprivation of driving license due to the drunk driving to be a valuable criterion to submit the applicant for the CDT assay during his qualifying as a driver.

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24

Girard, Donald E., Kusum L. Kumar, and John H. McAfee. "Hematologic Effects of Acute and Chronic Alcohol Abuse." Hematology/Oncology Clinics of North America 1, no. 2 (June 1987): 321–34. http://dx.doi.org/10.1016/s0889-8588(18)30678-6.

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25

Nixon, Sara Jo, and Julia A. Phillips. "Neurocognitive Deficits and Recovery in Chronic Alcohol Abuse." CNS Spectrums 4, no. 1 (January 1999): 95–102. http://dx.doi.org/10.1017/s109285290001124x.

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AbstractThe excessive and chronic use of alcohol is associated with a variety of neurocognitive changes in a substantial number of detoxified alcoholics. These deficits extend across a wide variety of neuropsychological domains and can be observed over a period of months following detoxification. Furthermore, they are seen in both male and female alcoholics, despite the fact that female alcoholics often have shorter drinking histories. Although these deficits are widely observed, there is considerable heterogeneity both within and across studies. Currently, the sources of this variability are only poorly understood. In this article, we review these neurocognitive and neurophysiological deficits, their pattern of recovery, potential contributing or confounding factors, and some of the clinical implications of these findings.

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26

Adams, C. "Anaesthetic implications of acute and chronic alcohol abuse." Southern African Journal of Anaesthesia and Analgesia 16, no. 3 (May 2010): 42–49. http://dx.doi.org/10.1080/22201173.2010.10872680.

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27

Kruman, Inna I., George I. Henderson, and Susan E. Bergeson. "DNA damage and neurotoxicity of chronic alcohol abuse." Experimental Biology and Medicine 237, no. 7 (July 2012): 740–47. http://dx.doi.org/10.1258/ebm.2012.011421.

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28

Setshedi, Mashiko, Jack R. Wands, and Suzanne M. de la Monte. "Acetaldehyde Adducts in Alcoholic Liver Disease." Oxidative Medicine and Cellular Longevity 3, no. 3 (2010): 178–85. http://dx.doi.org/10.4161/oxim.3.3.12288.

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Chronic alcohol abuse causes liver disease that progresses from simple steatosis through stages of steatohepatitis, fibrosis, cirrhosis, and eventually hepatic failure. In addition, chronic alcoholic liver disease (ALD), with or without cirrhosis, increases risk for hepatocellular carcinoma (HCC). Acetaldehyde, a major toxic metabolite, is one of the principal culprits mediating fibrogenic and mutagenic effects of alcohol in the liver. Mechanistically, acetaldehyde promotes adduct formation, leading to functional impairments of key proteins, including enzymes, as well as DNA damage, which promotes mutagenesis. Why certain individuals who heavily abuse alcohol, develop HCC (7.2–15%) versus cirrhosis (15–20%) is not known, but genetics and co-existing viral infection are considered pathogenic factors. Moreover, adverse effects of acetaldehyde on the cardiovascular and hematologic systems leading to ischemia, heart failure, and coagulation disorders, can exacerbate hepatic injury and increase risk for liver failure. Herein, we review the role of acetaldehyde adducts in the pathogenesis of chronic ALD and HCC.

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29

Purlik, I. L., V. M. Perelmuter, Ye V. Beloborodova та E. I. Beloborodova. "Сomparative morphological characteristics of activity score and fibrosis stage in chronic viral hepatitis C". Bulletin of Siberian Medicine 9, № 5 (28 жовтня 2010): 82–87. http://dx.doi.org/10.20538/1682-0363-2010-5-82-87.

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A comparison of degrees necroinflammatory activity and fibrosis stages in 433 biopsy specimens of patients with chronic viral hepatitis C (monoinfection and in combination with drug abuse, alcoholic disease, chronic opisthorchosis). Found that ethyl alcohol is the greatest character weights of alteration and severity of multiple sclerosis with HCV-infection. Drug abuse enhances fibrosis in the liver, but no histological activity, and only in comparison with mono-HCV infection. Opisthorchosis defines weakly expressed necroinflammatory and sclerotic changes with (by) HCV-infection.

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30

Cascella, Nicola G., Godfrey Pearlson, Dean F. Wong, Emmanuel Broussolle, Craig Nagoshi, Richard A. Margolin, and Edythe D. London. "Effects of Substance Abuse on Ventricular and Sulcal Measures Assessed by Computerised Tomography." British Journal of Psychiatry 159, no. 2 (August 1991): 217–21. http://dx.doi.org/10.1192/bjp.159.2.217.

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Computerised tomography (CT) was used to assess the possible effects of substance abuse on brain morphology. Polydrug abusers had significantly wider third ventricles than normal controls, with a positive correlation between age and ventricle:brain ratio (VBR). Assuming no effect of age, estimated quantity of substance abuse was not significantly related to ventricular and sulcal measures, except that alcohol consumption correlated positively with VBR and severity of cocaine use correlated negatively with sulcal width. When age of the subjects was partialled out, alcohol use showed a tendency for association with VBR; however, severity of cocaine use did not remain a significant predictor of cortical sulcal width. The findings suggest that chronic use of alcohol, but not necessarily of other commonly abused substances, produces brain atrophy.

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31

Krasemann, Thomas, and Sandra Klingebiel. "Influence of chronic intrauterine exposure to alcohol on structurally normal hearts." Cardiology in the Young 17, no. 2 (January 23, 2007): 185–88. http://dx.doi.org/10.1017/s1047951107000224.

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Abuse of alcohol during pregnancy is known to cause alcoholic embryopathy and congenital cardiac disease. We sought to establish if there were any cardiac abnormalities to be found in patients known to have alcoholic embryopathy, but with structurally normal hearts. We reviewed the electrocardiograms and echocardiographic data of 347 such patients without congenital cardiac disease. A shortened QT interval was found in half of the cases. The left ventricular diameter was small in one quarter of all patients, independent from age, gender, and the degree of alcoholic embryopathy. We conclude that intrauterine exposure to alcohol as a primary toxin can lead to minor cardiac abnormalities, even in the absence of structural congenital cardiac disease.

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Nawahir, Sultan, George Kurian, Thomas Alexander, and Susy Kurian. "Impact of alcohol on gastric mucosa in a population with high prevalence of Helicobacter pylori." International Journal of Advances in Medicine 8, no. 6 (May 26, 2021): 764. http://dx.doi.org/10.18203/2349-3933.ijam20212096.

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Background: The purpose of the study was to see whether chronic alcohol abuse had any effect on the gastric mucosa in a population already affected by a high prevalence of Helicobacter pylori.Methods: 35 males with a history of chronic alcohol abuse were compared with 35 males who were abstinent or social drinkers. All subjects had complaints of dyspepsia. All subjects underwent endoscopy and targeted biopsies were taken from three specific sites in the stomach, namely body, antrum and incisura. Biopsies were studied to look for changes of atrophic gastritis and intestinal metaplasia. The presence or absences of H. pylori on the tissue biopsy were also recorded.Results: Atrophic gastritis were only assessable in 24 alcoholic patients and 21 non-alcoholic patients due to the inadequacy of the depth of the biopsy. AG were found to be equally distributed in both the groups. 23 (64.9%) patients in the alcoholic group and 19(54.5%) in the control group had AG (OR-1.54, p=0.47). Intestinal metaplasia was seen in 10 (28.5%) alcoholic group and 12 (34.2) in the control group (OR-0.65, p=0.45). Of the 42 subjects detected to have AG, 16 (38.1%) had IM. However, IM were always associated with AG. In addition, H. pylori were not seen to be different in the two groups. H. pylori were positive in 18 (51.4%) alcoholic and14 (40%) non-alcoholic patients (p=0.33).Conclusions: Chronic alcohol abuse doesn’t appear to have any major impact on the gastric mucosa in terms of producing premalignant lesions such as atrophic gastritis or intestinal metaplasia or enhancing the prevalence of H. pylori.

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33

Kalezic, Nevena, Milica Karadzic-Kocica, Nemanja Dimic, Mladen Kocica, Anka Toskovic, Milan Jovanovic, and Ivan Dimitrijevic. "Alcohol abuse as a risk factor for developing thyroid cancer." Srpski arhiv za celokupno lekarstvo, no. 00 (2020): 113. http://dx.doi.org/10.2298/sarh201123113k.

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Introduction/Objective. Alcohol abuse influence on developing thyroid cancer is controversial. While some studies consider it a protective factor, others deny any impact on thyroid cancer. The objective of the paper was to establish a possible link between alcohol abuse and certain types of thyroid cancers. Methods. The retrospective study included 502 patients with thyroid cancer and control group of 600 patients with benign forms of thyroid diseases (e.g. nodular, multinodular and toxic nodular goiter). Thyroid cancer patients were divided into 4 groups: I - papillary, II - medullary, III - anaplastic, and IV - follicular carcinoma, and grouped by sex, age (< 30 yrs.; > 30 yrs.) and alcohol abuse, as defined by WHO. Results. Thyroid cancer patients were predominantly male of younger age. This distribution difference was statistically significant in groups I and II (p < 0.001). Of total 10 (0.9%) patients with chronic alcohol abuse, 8 (1.6%) had thyroid cancer, while 2 (0.3%) belonged to the control group (p < 0.001). In thyroid cancer patients, chronic alcohol abuse was absent in group III and IV. Distribution in group I and II was 6 (1.6%) and 2 (2%) respectively (p < 0.001). Conclusion. Alcohol abuse deserves to be considered as a risk factor for papillary and medullary forms of thyroid cancer, while it does not stay the same for anaplastic and follicular thyroid cancers.

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34

Schwan, R., and M. Reynaud. "Intravenous lorazepam reduced alcohol related seizures in patients with chronic alcohol abuse." Evidence-Based Mental Health 2, no. 4 (November 1, 1999): 107. http://dx.doi.org/10.1136/ebmh.2.4.107.

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35

Boloursaz, Samine, Sirous Nekooei, Farrokh Seilanian Toosi, Hossein Rezaei-Dalouei, Behrooz Davachi, Sahar Kazemi, and Bita Abbasi. "Marchiafava-Bignami and Alcohol Related Acute Polyneuropathy: The Cooccurrence of Two Rare Entities." Case Reports in Neurological Medicine 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/5848572.

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Objectives. The aim of this article is to represent the first reported case with cooccurrence of two rare alcohol related complications.Case Report. We report a 38-year-old man with chronic alcoholism who presented with both cranial and peripheral nerve palsy. On MRI examination characteristic findings of Marchiafava-Bignami disease were recognized.Discussion. Marchiafava-Bignami disease (MBD) is a rare complication of long-term, heavy alcohol abuse that has characteristic MRI findings. Acute alcohol related polyneuropathy (AARP) is another rare and not-well-understood complication of chronic alcohol abuse. We could not find any previous report of the cooccurrence of these two complications in the literature.

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Machado, Ísis Eloah, Francisco Carlos Félix Lana, Mariana Santos Felisbino-Mendes, and Deborah Carvalho Malta. "Factors associated with alcohol intake and alcohol abuse among women in Belo Horizonte, Minas Gerais State, Brazil." Cadernos de Saúde Pública 29, no. 7 (July 2013): 1449–59. http://dx.doi.org/10.1590/s0102-311x2013000700018.

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The main objective of this cross-sectional study was to analyze factors associated with alcohol consumption among adult women living in Belo Horizonte, Minas Gerais State, Brazil, in 2011. Data for Belo Horizonte were obtained from the VIGITEL system (Telephone-Based Surveillance of Risk and Protective Factors for Chronic Diseases). Alcohol use was defined as self-reported intake of at least one dose in the previous 30 days; alcohol abuse was defined as four or more doses on at least one occasion during the same period. Polytomous logistic regression was used to evaluate factors associated with alcohol use and abuse. Alcohol use was more prevalent among women 25 to 34 years of age. Alcohol abuse was associated with age, schooling, health status, and smoking. The results suggest the need for policies to prevent alcohol abuse among women, especially targeting those who are younger, single, smokers, and with more education.

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Thota, Darshan, and Sherri Rudinsky. "Wernicke’s Encephalopathy in a Patient Without Chronic Alcohol Abuse." Clinical Practice and Cases in Emergency Medicine 1, no. 2 (March 14, 2017): 95–97. http://dx.doi.org/10.5811/cpcem.2016.12.32769.

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38

Lindgren, S., B. Lilja, H. Verbaan, and G. Sundkvist. "Alcohol Abuse Exaggerates Autonomic Dysfunction in Chronic Liver Disease." Scandinavian Journal of Gastroenterology 31, no. 11 (January 1996): 1120–24. http://dx.doi.org/10.3109/00365529609036897.

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39

Canan, Faith, and Ahmet Ataoglu. "Panic Disorder After the End of Chronic Alcohol Abuse." Primary Care Companion to The Journal of Clinical Psychiatry 10, no. 04 (August 15, 2008): 332–33. http://dx.doi.org/10.4088/pcc.v10n0411d.

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40

Moss, Marc. "Epidemiology of Sepsis: Race, Sex, and Chronic Alcohol Abuse." Clinical Infectious Diseases 41, Supplement_7 (November 15, 2005): S490—S497. http://dx.doi.org/10.1086/432003.

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41

Farris, S. P., D. Arasappan, S. Hunicke-Smith, R. A. Harris, and R. D. Mayfield. "Transcriptome organization for chronic alcohol abuse in human brain." Molecular Psychiatry 20, no. 11 (December 2, 2014): 1438–47. http://dx.doi.org/10.1038/mp.2014.159.

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42

Lamberts, H. "PATIENTS WITH CHRONIC ALCOHOL ABUSE IN DUTCH FAMILY PRACTICES." Alcohol and Alcoholism 34, no. 3 (May 1, 1999): 337–45. http://dx.doi.org/10.1093/alcalc/34.3.337.

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43

Augustyńska, B., A. Araszkiewicz, G. Odrowąż-Sypniewska, L. Grodzki, and J. Sobczyk. "Monocyte Chemotactic Protein - 1 (MCP-1) Concentration in Alcohol Dependent Women." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70639-x.

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Background:Prolonged alcohol abuse as a chronic disease may increase inflammation and lead to hepatic disorders. Liver fibrosis results from chronic damage to the liver in conjunction with the accumulation of ECM proteins, which is characteristic of most types of chronic liver diseases. The main cause of liver fibrosis include alcohol abuse. The pathological features of hepatic cirrhosis induced by ethanol and other factors are similar. Monocyte chemotactic protein - 1 (MCP-1) is a protein related to inflammation and fibrosis.The aim of this study was to assess of MCP-1in serum of alcohol dependent women.Methods:Study group consisted of 40 inpatients treated in Inpatients Clinic in Toruń. Mean age of females in the study group was 43+/-7 yrs, duration of alcohol dependence 8+/-6 yrs. Control group consisted of 35 healthy women. Monocyte chemotactic protein - 1 (MCP-1) in the serum was determined by ELISA, serum AST and ALT on automatic analyzer.Results:Average serum AST was 32,88+/-32,95, ALT 29,76+/-24,48 (U/l). The concentration of MCP-1 was significantly higher in alcohol-dependent female group compared to healthy subjects (360,34ng/ml +/-273,95 vs 240,27ng/ml+/-178,31; p=0,030).Conclusions:These results imply that prolonged alcohol abuse leads to increased concentrations of MCP-1 and may in consequence have impact on the pro-inflammatory state related to increased risk of liver fibrosis. Our results suggests that prolonged alcohol abuseas as chronic disease can be a factor of inflammation and lead to hepatic disorders.

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44

Dolan, Vera. "Low Serum Creatinine as a Marker for Undisclosed Alcohol Abuse." Journal of Insurance Medicine 49, no. 2 (February 22, 2022): 114–16. http://dx.doi.org/10.17849/insm-49-2-1-3.1.

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Detecting undisclosed alcohol abuse in life insurance applicants has always been a challenge to life underwriters and medical directors. This case report describes a 38-year-old woman with classic signs, symptoms, behavior and biochemical markers of undisclosed alcohol abuse. Review of 10 years of medical records revealed chronic abnormally low serum creatinine results associated with abnormally elevated liver function tests, and repeated denials to attending physicians of ever consuming alcohol. Kidney function throughout the 10-year history was not impaired. Low serum creatinine may be a good marker for detecting undisclosed alcohol abuse, but only when there is no kidney injury, dysfunction or impairment obscuring it.

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Matsumoto, Kazu, Hiroyasu Ogawa, and Haruhiko Akiyama. "Multifocal Osteonecrosis Secondary to Chronic Alcohol Ingestion." Case Reports in Orthopedics 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/137273.

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Multifocal osteonecrosis is a relatively rare disorder with an estimated incidence of around 3% among patients diagnosed as having osteonecrosis. Multifocal osteonecrosis is caused by the several conditions including corticosteroid treatment, coagulation disorders, connective tissue disorders including systemic lupus erythematosus (SLE), inflammatory bowel disease, renal transplantation, and underlying malignancies. Alcohol abuse is one of the risk factors for osteonecrosis, and alcohol-induced osteonecrosis is 5% among all the osteonecrosis. Furthermore, the overall incidence of alcohol-induced multifocal osteonecrosis was approximately 6% among all the osteonecrosis induced by the alcohol. Therefore, here, we report an extremely rare case of alcohol-induced multifocal osteonecrosis involving three joints (two knees and one hip) and review the related literature.

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Nichols, Whitney, and Angela Amedee. "Direct effects of alcohol on the mucosal barrier and the implications on HIV transmission (MUC2P.935)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 65.18. http://dx.doi.org/10.4049/jimmunol.194.supp.65.18.

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Abstract Alcohol abuse is associated with an increased risk of HIV sexual transmission; however, the biological changes in the genital tract are unknown. The first line of defense is provided by the cervicovaginal epithelium acting as a physical barrier to infection. The epithelial cell innate properties are affected by various factors within the genital milieu. We hypothesize that alcohol abuse compromises cervicovaginal epithelial barrier function resulting in enhanced penetration of HIV to the underlying submucosa. Using a vaginal epithelial cell line grown at an air-liquid interface in a transwell, we modeled chronic alcohol exposure by supplementing the basolateral media with physiologically relevant levels of ethanol (50 mM). Epithelium barrier disruption was evident in the alcohol-treated cells by a significant decrease in TEER (p=0.001) and an increased permeability to 10kDa FITC-dextran (p=0.01) relative to control. Cell viability was unaffected by chronic alcohol exposure. Epithelial cells of the female genital tract exhibit significant changes in physical barrier integrity after exposure to intoxicating levels of alcohol. These changes in epithelial cell innate properties provide evidence for a biological mechanism of enhanced HIV penetration and infection in women who abuse alcohol. Future studies in alcohol-exposed cell culture models of both the upper and lower genital mucosa will identify specific mechanisms of HIV transmission.

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Shenkman, Boris S., Olga E. Zinovyeva, Svetlana P. Belova, Timur M. Mirzoev, Natalia A. Vilchinskaya, Ivan M. Vikhlyantsev, Anna D. Ulanova, et al. "Cellular and molecular signatures of alcohol-induced myopathy in women." American Journal of Physiology-Endocrinology and Metabolism 316, no. 5 (May 1, 2019): E967—E976. http://dx.doi.org/10.1152/ajpendo.00513.2018.

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Alcoholic myopathy is characterized by the reduction in cross-sectional area (CSA) of muscle fibers and impaired anabolic signaling. The goal of the current study was to investigate the causes and compare the changes in CSA and fiber type composition with the modifications of anabolic and catabolic signaling pathways at the early stages of chronic alcohol consumption in women. Skeletal muscle samples from 5 female patients with alcohol abuse (AL; 43 ± 5 yr old; alcohol abuse duration 5,6 ± 0,6 yr) were compared with the muscle from the control group of 8 healthy women (C; 35 ± 4 yr old). The average daily dose of alcohol consumption was 110 ± 10 ml of pure ethanol. In women patients, a significant decrease in CSA of type I and II muscle fibers, titin and nebulin content, plasma IGF-1 level and total IRS-1, p-Akt and p-4E-BP1 in vastus lateralis was found in comparison with the control group. The p-AMPK level was found to be increased versus the control group. In women patients with chronic alcoholic myopathy 1) both fast and slow muscle fibers are subjected to atrophy; 2) impairments in IGF-I-dependent signaling and pathways controlling translation initiation (AMPK/mTOR/4E-BP1), but not translation elongation, are observed; 3) the level of calpain-1 and ubiquitinated proteins increases, unlike E3 ligases content.

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Harchenko, O., O. Savchuk, and L. Ostapchenko. "Analysis of protein profile changes in chronic alcohol intoxication to diagnose the development of these pathological conditions." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 70, no. 2 (2015): 11–19. http://dx.doi.org/10.17721/1728_2748.2015.70.11-19.

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In the review it was characterized today existing biomarkers that allow to detect chronic alcohol abuse, namely: carbohydrate-deficient transferrin, the activity of GGT, ALT, AST, β-hexosaminidase; sialic acid index of apolipoprotein J, circulating levels of cytokines (TNF-α, IL-1 and IL-6), α-1- and α-2 globulins, serum amyloid A4, fibronectin, and others. At present results of the studies of alcohol abusers organism's proteome contain significant amount of artifacts, which are connected with the other substances of double abuse (e.g. cocaine, tobacco), specific nutrition deficiency, and the presence of organs dysfunction. Summarising the scientific literature analysis we can attest the lack of research concerning proteome changes at different stages of alcohol intoxication. An important task is to identify biomarkers that would allow measuring the level of alcohol consumption by detecting tissue damage and other physiological reactions on the alcohol abuse over time. Strategies of alcoholism biomarkers research should include the identification of proteins, which number differs in alcoholics and non-alcoholics. Decoding of individual proteome is likely to be part of the future personalized medicine.

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Sandi, Yudisa Diaz Lutfi, Lina Nurul Hidayati, and Hamidatus Daris. "Alcohol Consumption Motivation in Adolescents." Jurnal Ners dan Kebidanan (Journal of Ners and Midwifery) 8, no. 2 (August 12, 2021): 171–77. http://dx.doi.org/10.26699/jnk.v8i2.art.p171-177.

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The number of alcoholic drinks that adolescents abuse was due to various reasons. The objective of the study was to explore the motivation of adolescents in consuming alcohol. This study used a qualitative descriptive method. 13 participants were selected according to the inclusion criteria using snowball sampling. The data collection used semi-structured interviews. The data analysis stage in this study used the Colaizzi technique. This study consisted 3 main themes and 19 sub-themes; (1) feelings: a) comfortable, b) happiness, c) relieved, d) satisfied; (2) encouragement: a) society, b) curious, c) addictive, d) friend invitation, e) escape, f) solidarity, g) got trouble, h) stimulate activity, i) looking for new experience; (3) achievement: a) got many friends, b) recognized, c) so it looks cool, d) he problem solved, e) able to tell stories, f) healthy in body. The consumption of alcohol in adolescents was based on the will of the adolescent, both from within the individual and from outside the individual which motivated adolescents to consume alcohol with a purpose that the individual believes. Alcohol abuse among adolescents is a chronic problem in the government's efforts to reduce numbers due to the effect of alcoholic drinks. Alcoholic drink is a type of drink that has an intoxicating effect, is dependent on nature and causes changes in behavior, perceptions, emotions and cognition for those who consume it

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Lin, Song-Chow, Yun-Ho Lin, Chin-Fa Chen, Chia-Yu Chung, and Shih-Hsien Hsu. "The Hepatoprotective and Therapeutic Effects of Propolis Ethanol Extract on Chronic Alcohol-induced Liver Injuries." American Journal of Chinese Medicine 25, no. 03n04 (January 1997): 325–32. http://dx.doi.org/10.1142/s0192415x97000366.

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Propolis designates a mixture of gums, resins and balms, of viscous consistency, which are gathered on certain parts (buds and bark, mainly) of vegetables (especially coniferous trees) by honeybees. They bring this back to the hive, where it is modified and mixed with other substances (essentially their own wax and salivary secretions). In this study, the hepatoprotective and therapeutic effects of propolis ethanol extract on chronic alcohol-induced liver injuries were investigated in rats. 3.125 ml of 99.5% alcohol was added to animal's daily diet for four weeks to induce chronic alcohol liver injuries. After sacrifice, serum transaminases (GOT, GPT), triacylglyceride and hepatic triacylglyceride (HTG) concentration were assayed to observe liver injuries induced by chronic alcohol abuse. In addition, the phenomenon of alcohol induced fatty liver were also observed by histopathological changes. Different doses of propolis ethanol extract were p.o. administered three times per day for three days, after four weeks' alcohol administration. It was found that 10 mg/kg of propolis ethanol extract significantly decreased the elevations of serum GOT, GPT, TG and HTG. In histopathological examination, 30 mg/kg of propolis ethanol extract also remarkably decreased the hepatocellular fatty degeneration, apparent as vacuolization, induced by chronic alcohol abuse.

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