Alcohol Withdrawal Syndrome

Carlson, Richard W.; Kumar, Nivedita N.; Wong-Mckinstry, Edna; Ayyagari, Srikala; Puri, Neerja; Jackson, Frank K.; Shashikumar, Shivaramaiah

doi:10.1016/j.ccc.2012.07.004

Cited by 134 publications

(75 citation statements)

References 200 publications

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“…Recent studies also implicate the potential of preconception paternal alcohol consumption, which can lead to FASD (Kim et al, 2014;Knezovich and Ramsay, 2012). Previous studies have shown the importance of both alcohol exposure and withdrawal (termination of alcohol consumption) in FASD pathogenesis (Carlson et al, 2012), emphasizing the necessity to study the effect of both ethanol exposure and withdrawal on the central nervous system development (Pierog et al, 1977;Thomas and Riley, 1998). During development, "binge-like" (single time) ethanol exposure as well as continuous ethanol exposure are reported to cause severe effects that contribute to FASD pathobiology (Flegel et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Ethanol deregulates Mecp2/MeCP2 in differentiating neural stem cells via interplay between 5-methylcytosine and 5-hydroxymethylcytosine at the Mecp2 regulatory elements

Liyanage

Zachariah

Davie

et al. 2015

Experimental Neurology

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Methyl CpG Binding Protein 2 (MeCP2) is an important epigenetic factor in the brain. MeCP2 expression is affected by different environmental insults including alcohol exposure. Accumulating evidence supports the role of aberrant MeCP2 expression in ethanol exposureinduced neurological symptoms. However, the underlying molecular mechanisms of ethanolinduced MeCP2 deregulation remain elusive. To study the effect of ethanol on Mecp2/MeCP2 expression during neurodifferentiation, we established an in vitro model of ethanol exposure, using differentiating embryonic brain-derived neural stem cells (NSC). Previously, we demonstrated the impact of DNA methylation at the Mecp2 regulatory elements (REs) on Mecp2/ MeCP2 expression in vitro and in vivo. Here, we studied whether altered DNA methylation at these REs is associated with the Mecp2/MeCP2 misexpression induced by ethanol. Binge-like and continuous ethanol exposure upregulated Mecp2/MeCP2, while ethanol withdrawal downregulated its expression. DNA methylation analysis by methylated DNA immunoprecipitation indicated that increased 5-hydroxymethylcytosine (5hmC) and decreased 5-methylcytosine (5mC) enrichment at specific REs were associated with upregulated Mecp2/MeCP2 following continuous ethanol exposure. The reduced Mecp2/MeCP2 expression upon ethanol withdrawal was associated with reduced 5hmC and increased 5mC enrichment at these REs. Moreover, ethanol altered global DNA methylation (5mC and 5hmC). Under the tested conditions, ethanol had minimal effects on Authors' contributionsVichithra R.B. Liyanage: Conception and design, collection and assembly of data, data analysis and interpretation, manuscript writing, and final approval of manuscript. Robby M. Zachariah: Conception and design, collection and assembly of data, and final approval of manuscript. James R. Davie: Scientific input, manuscript revisions, and final approval of manuscript. Mojgan Rastegar: Conception and design, contributed reagents/materials/analysis tools, data analysis and interpretation, manuscript writing, and final approval of manuscript. Conflict of interest statement

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Section: Introductionmentioning

confidence: 99%

Ethanol deregulates Mecp2/MeCP2 in differentiating neural stem cells via interplay between 5-methylcytosine and 5-hydroxymethylcytosine at the Mecp2 regulatory elements

Liyanage

Zachariah

Davie

et al. 2015

Experimental Neurology

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“…Brief comments on the reasons for the administration of each drug in the pharmacotherapy of alcohol intoxication treatment are also included in Tables III and IV (Carlson et al, 2012). The few unwanted events resulting from these associations may have contributed to the cases of death previously described in our research.…”

Section: Resultsmentioning

confidence: 81%

Prevalence and risk of potentially adverse drug interactions in the treatment of acute alcohol poisoning

Andrade

Rocha

Maciel

et al. 2016

Braz. J. Pharm. Sci.

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The aim of this paper is to determine the profile of acute alcohol poisoning and to estimate the risk of potentially adverse drug interactions (ADIs) in patients intoxicated by alcohol when attended in emergency care at hospital. A descriptive serial cross-sectional study was performed with 4,271 individuals intoxicated by alcohol, from January 2009 to July 2011. Possible correlations were measured by Pearson's chi-square test. The data show high consumption in the population, especially in males between 25 and 59 years. The main circumstances for poisoning were alcohol misuse (96.3%). After treatment complete recovery from the signs or symptoms of the poisoning was observed in 96.88% cases; and death in 0.70%. The demonstration of potential risk for ADIs in medical care included 300 medical records which contained a history of acute alcohol poisoning. Possible drug-drug interactions (44.2%) and drug-alcohol interactions (55.8%) were demonstrated in 60.60% of analyzed medical records. Among these cases, 3%, 92.4% and 4.6% were classified as mild, moderate and severe, respectively. The measurement of ADIs aims to prevent clinical complications in medical care for alcohol misuse disorders.Uniterms: Alcoholic intoxication. Emergency Medical Services. Risk Management. Medicines/adverse interactions/risk control. Medicines/alcohol interactions/risk control. O objetivo deste trabalho foi definir o perfil de intoxicação alcoólica aguda e estimar o risco de interações medicamentosas adversas (IMAs) potenciais em pacientes com intoxicação alcoólica atendidos na emergência hospitalar. Um estudo descritivo, serial, de corte transversal foi realizado com 4.271 indivíduos com intoxicação alcoólica, de janeiro 2009 a julho 2011. Correlações foram medidas pelo teste qui-quadrado. Os dados mostram alto consumo na população estudada, especialmente em homens de 25 a 59 anos. A principal circunstância de intoxicação foi o abuso (96,3%). Após tratamento, cura foi observada em 96,88% dos casos e morte em 0,7%. O risco de IMAs potenciais no atendimento médico incluiu 300 prontuários médicos com histórico de intoxicação alcoólica aguda. Possíveis interações medicamentosas (44,2%) e interações fármaco-álcool (55,8%) foram observadas em 60,6% dos prontuários analisados. Entre elas, 3%, 92,4% e 4,6% foram classificadas como leve, moderada e grave, respectivamente. A medição das IMAs visa a prevenir complicações clínicas no atendimento dos agravos devido ao abuso de álcool.Unitermos: Intoxicação alcoólica. Serviços Médicos de Emergência. Medicamentos/interações adversas/ controle de risco. Medicamentos/interação com álcool/controle de risco.

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“…6 Benzodiazepines including lorazepam, diazepam and midazolam are the most commonly used and recommended agents for AWS. 4 Though the benzodiazepines have shown to be effective, increasing doses of BZDs place a patient at a risk of respiratory depression. So in a patient with AWS, BZD monotherapy may not be effective enough to control symptoms and may worsen delirium.…”

Section: Disscusionmentioning

confidence: 99%

Add on dexmedetomidine in the treatment of severe alcohol withdrawal in a patient of emergency laparotomy

Shende¹,

Ambare²,

Bachewar³

et al. 2015

Int J Res Med Sci

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Alcohol Withdrawal Syndrome

Cited by 134 publications

References 200 publications

Ethanol deregulates Mecp2/MeCP2 in differentiating neural stem cells via interplay between 5-methylcytosine and 5-hydroxymethylcytosine at the Mecp2 regulatory elements

Ethanol deregulates Mecp2/MeCP2 in differentiating neural stem cells via interplay between 5-methylcytosine and 5-hydroxymethylcytosine at the Mecp2 regulatory elements

Prevalence and risk of potentially adverse drug interactions in the treatment of acute alcohol poisoning

Add on dexmedetomidine in the treatment of severe alcohol withdrawal in a patient of emergency laparotomy

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