md-medicaldata

Authors

 

Neykova - Vasileva Lyudmila<sup>1

1</sup> Clinic of Emergency Toxicology, Military Medical Academy, Sofia

 

UDK: 616-074-056.85:613.81

The paper recieved/ Rad primljen: 10.04.2018.

Accepted / Rad prihvaćen: 05.05.2018.

 

Correspondent to

Assist. prof. Neykova - Vasileva Lyudmila, MD,PhD
Clinic of Emergency Toxicology, Military Medical Academy
Georgi Sofiiski 3, Sofia 1606, Bulgaria
e-mail: laneykova@abv.bg

 

 

Abstract

 

The Alcohol withdrawal syndrome (AWS) reflects the neuro-biochemical adaptation of the organism to recurrent alcohol consumption and the symptoms are opposite of those caused by the substance. The core of the multiple abstinence pathology consists of changes in neuro-mediators. Ethanol rapidly crosses the blood-brain barrier and affects membranes, ion channels, enzymes and central nervous system (CNS) neurons.The material aims to analyze the data in the literature about the influence of the chronic alcohol use on the catecholamine levels, which are the basis for the intensity and duration of the alcohol withdrawal syndrome.To conclude: the catecholamine neurotransmission is the basis for the various symptoms of ethanol withdrawal. All patients with alcohol addiction develop AWS. Their pathogenesis is the plasma levels of adrenaline and noradrenaline. AWS is often of a short duration, but can quickly enter into a pre-delirium or delirium. In the pre-crisis period, the somatic manifestations are discrete – light tremor, tendency to tachycardia, minor increase in blood pressure (BP), skin moistening. It is during this period that an active observation is needed to capture these prodromal signs. In the meantime, the onset of treatment often prevents the onset of delirium tremens.

 

 

Key words:

alcohol, withdrawal syndrome, mediators in the central nervous system, catecholamine’s

 

 

Sažetak

 

Alkoholni apstinentski sindrom je odraz neurobiohemijske adaptacije organizma na ponovljenu konzumaciju alkohola, a simptomi koji se javljaju su suprotni onima koji su uzrokovani supstancom. Razlog apstinentske pojave nalazi se u promenama u neuromedijatorima. Etanol brzo prelazi krvno-moždanu barijeru i utiče na membrane, jonske kanale, enzime i neurone centralnog nervnog sistema (CNS). Cilj rada je analiza podataka u literaturi o uticaju hroničnog korišćenja alkohola na nivoe kateholamina, koji su osnova intenziteta i trajanja alkoholnog apstinentskog sindroma. Da zaključimo: neurotransmisija kateholamina je osnova za razne simptome alkoholne apstinencije. Svi pacijenti sa zavisnošću od alkohola razvijaju alkohlni apstinentski sindrom. Za patogenezu ovog oboljenja su odgovorni nivoi adrenalina i noradrenalina u plazmi. Apstinentski sindrom je često kratkog trajanja, ali može brzo ući u pre-delirium ili delirijum. U periodu pre krize, somatske manifestacije su diskretne - blagi tremor, tendencija ka tahikardiji, blago povećanje krvnog pritiska, vlaženje kože. Tokom ovog perioda potrebno je aktivno posmatranje kako bi se uhvatili ovi prodromalni znaci. U međuvremenu, početak lečenja često sprečava pojavu delirium tremensa.

 

 

Ključne reči:

alkohol, apstinentski sindrom, medijatori u centralnom nervnom sistemu, kateholamini

 

 

Bibliography:

 

1. Schuckit, M.A. (2006). ed.6. Drug and alcohol abuse: a clinical guide to diagnosis and treatment. New York, Springer; 1897-1904;
2. Eyer, F., T. Schuster, et al. Risk assessment of moderate to severe alcohol withdrawal–predictors for seizures and delirium tremens in the course of withdrawal. Alcohol Alcohol, 2011, 46(4): 427-433;
3. Esel, E. (2006). "Neurobiology of alcohol withdrawal inhibitory and excitatory neurotransmitters." Turk Psikiyatri Derg 17(2): 129-37;
4. De Witte P., E. Pinto et al. (2003). "Alcohol and withdrawal: from animal research to clinical issues." Neu­rosci Biobehav Rev 27(3): 189-97; 
5. Uzbay T.I. "Atypical Antipsychotic Drugs and Ethanol Withdrawal Syndrome: A Review." Alcohol Alcohol. 2012 Jan-Feb;47(1):pp.33-41;
6. Энтин Г.М. Лечение алкоголизма. Москва, „Медицина”, 1990, стр. 28-31; 
7. Lieber CS: Metabolic effects of acetaldehyde.1988,  Biochem Soc Trans 16, 241-247;
8. Eyer, F., T. Schuster, et al. Risk assessment of moderate to severe alcohol withdrawal–predictors for seizures and delirium tremens in the course of withdrawal. Alcohol Alcohol, 2011, 46(4): 427-433;
9. Oreland L (January 2004). "Platelet monoamine oxidase, personality and alcoholism: the rise, fall and resurrection". Neurotoxicology. 25 (1–2): 79–89;
10. Evan E. Bolton; Yanli Wang; Paul A. Thiessen; Stephen H. Bryant (2008). „Chapter 12 PubChem: Integrated Platform of Small Molecules and Biological Activities”. Annual Reports in Computational Chemistry. 4: 217—241;
11. McKeon A., M.A. Frye, et al. (2008). "The alcohol withdrawal syndrome." J. Neurol Neurosurg Psy­chiatry 79(8): 854-62;
12. Strat Y.L., N. Ramoz et al. (2008). "Molecular genetics of alcohol dependence and related endo­phe­no­types." Curr Genomics 9(7): 444-51;
13. Morikawa H., R.A. Morrisett (2010). "Ethanol action on dopaminergic neurons in the ventral tegmental area: interaction with intrinsic ion channels and neurotransmitter inputs." Int Rev Neurobiol 91: 235-88;
14. Gauthier PM, Szerlip HM.Metabolic acidosis in the intensive care unit. Crit Care Clin 2002;18:289–308;
15. Bondy S.C. Ethanol toxicity and oxidative stress. Toxicology Letters. Vol. 63, Issue 3, December 1992, pp. 231-241;
16. Zakhari S. Overview: how is alcohol metabolized by the body? Alcohol Res Health 2006; 29: 245-257;
17. Taganovich A.D., Oletskiy E.I., Kotovich I.L. Patologicheskaya biokhimiya [Pathological Bioche­mistry]. Moscow: Binom, 2013, 448 p.;         
18. Bogdanova I.V. The role of dopamine in the mechanisms of formation of certain CNS disorders and conditions of dependence: a review of literature, Ukrainskiy vestnik psikhonevrologii, 2011, no. 19, iss. 2 (67), pp. 5-8;
19. Swaminathan R. Magnesium metabolism and its disorders. Cllin Biochem Rev 2003; 24: 47–66;   
20. Kekelidze Z.I., Zemskov A.P., Filimonov B.A. Heavy delirium tremens, Russkiy meditsinskiy zhurnal, 1998, № 2, pp. 103-108;
21. Goldberg A. L. (1995). Functions of the proteasome: the lysis at the end of the tunnel. Science 268: 522-523;
22. Shabanov P.D., Kalishevich S.Yu. Biologiya alkogolizma [Biology of alcoholism]. Saint-Petersburg: Lan, 1998. 272 p.;
23. Yu P.M., Tipton T.F., Boultan A.A. Current neurochemical and pharmacological aspects of biogenic amines. Elsevier Science Pub Co, 1995, 372p.;
24. Netter P, Vogel WH. he effect of drinking habit on catecholamine and behavioral responses to stress and ethanol. Neuropsychobiology, 1990-1991;24(3):149-58;
25. Gessa et al. 1985. Gessa GL, Muntoni F, Collu M, Vargiu L, Mereu G. Low doses of ethanol activate dopaminergic neurons in the ventral tegmental area. Brain Res 348: 201–203;
26. Young SN (2007). «How to increase serotonin in the human brain without drugs». Rev. Psychiatr. Neurosci. 32 (6): 394–99;
27. Droblenkov AV. Morphological signs of ethanol poisoning, alcohol abstinence and chronic alcoholic in­to­xication in the mesocorticolimbic dopaminergic system.// Sudebno-Meditsin skaia Ekspertiza. 2011 Sep-Oct. 54 (5):11-7;
28. Nenadic SK., Nedic G., Nikolac M., Mustapic M., Muck-Seler D., Borovecki F., Pivac N. Insomnia, pla­telet serotonin and platelet monoamine oxidase in chronic alcoholism. // Neuroscience Letters, 2011 Aug 18, 500(3): 172-6;
29. Анохина И.П. Регуляция функции дофаминовой системы как основа разработки новых методов лечения алкоголизма. Первый съезд психиатров социалистических стран, Москва, 1987;стр. 402-407;
30. Strat Y.L., N. Ramoz et al. (2008). "Molecular genetics of alcohol dependence and related endopheno­types." Curr Genomics 9(7): 444-51;
31. Tambour S., E. Quertemont (2007). "Preclinical and clinical pharmacology of alcohol dependence." Fundam Clin Pharmacol 21(1): 9-28;
32. Bowirrat A., Oscar-Berman M. Relationship between dopaminergic neurotransmission, alcohollism, and Reward Deficiency syndrome. // American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: the Official Publication of the International Society of Psychiatric Genetics. 2005 Jan 5, 132B (1): 29-37.

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