Contagem de leucócitos e morbimortalidade no infarto do miocárdio / Leukocyte count and morbimortality in myocardial infarction

Objetivo: Avaliar a associação entre maiores níveis da contagem total de leucócitos periféricos e relação neutrófilos/linfócitos obtidos na admissão hospitalar, bem como a morbimortalidade em pacientes diagnosticados com infarto do miocárdio. Métodos: Avaliamos 276 pacientes com infarto agudo do miocárdio, entre janeiro de 2014 e novembro de 2015. Os dados clínicos e laboratoriais foram obtidos e relacionados a: internação, complicações intra-hospitalares, readmissões e mortalidade em 30 dias pós-internação. Resultados: A idade média foi 61 anos e 66,7% eram homens. Pacientes com complicações, comparados ao grupo sem complicações, eram mais velhos (60,85 vs. 62,54; p=0,053), tinham níveis de leucócitos (10,23 vs. 11,78; p=0,001) e neutrófilos (7,17 vs. 8,38; p=0,020) aumentados, doença multiarterial (38,2% vs. 74,5%; p<0.001) e supradesnivelamento de ST (49,3 vs. 65,1; p=0,039). Dois grupos foram constituídos pela mediana (10,56) dos leucócitos e demonstraram-se incidências mais elevadas de choque cardiogênico (p<0,001) e mortes (p=0,031) no grupo com maior leucocitose. Houve associação significativa entre leucócitos >10,56 e valores superiores de CK-MB (p=0,001) e troponina (p=0,039). Conclusão: Houve associação entre aumento dos níveis de leucócitos e maior incidência de complicações intra-hospitalares, incluindo morte, até 1 mês após alta hospitalar em pacientes com infarto agudo do miocárdio. A contagem de leucócitos mostrou relação mais evidente do que a relação neutrófilos/linfócitos e sua fácil acessibilidade colocá-o como ferramenta útil para determinação do prognóstico em pacientes com infarto do miocárdio.(AU)

Objective: To evaluate the association of higher levels of total peripheral leukocytes count and neutrophil/lymphocyte ratio at admission, as well as morbidity and mortality in patients diagnosed with myocardium infarction. Methods: We evaluated 276 patients with Acute Myocardial Infarction through January 2014 to November 2015. Clinical and laboratory data were obtained and related to hospital stay, inhospital complications, 30 day readmissions and mortality. Results: The average age was 61 years, 66.7% were male. Patients with complications, compared to the group with no complications, are older (60.85 vs 62.54, p=0.053), had increased levels of leucocytes (10.23 vs 11.78, p=0.001) and neutrophils (7.17 vs 8.38, p=0.020) count, multivessel disease (38.2% vs 74.5%, p<0.001) and ST elevation (49.3 vs 65.1, p=0.039). Two groups were formed by leucocyte median, and a higher incidence of cardiogenic shock (p<0.001) and deaths (p=0.031) was shown in the group with higher leuco cytosis. There was significant association between leucocytes >10.56 and higher CKMB (p=0.001) and troponin (p=0.039) values. Conclusion: Our study confirms an association between increased levels of leucocytes count and higher incidence of inhospital complications, including death, up to one month after hospital discharge in patients with acute myocardial infarction. Leucocytes count showed a more evident relation than neutrophil/lymphocyte ratio, and its easy accessibility poses it as a very useful tool to determine prognosis in patients with myocardial infarction.(AU)

A review on alcohol: from the central action mechanism to chemical dependency.

INTRODUCTION: alcohol is a psychotropic depressant of the central nervous system (CNS) that promotes simultaneous changes in several neuronal pathways, exerting a profound neurological impact that leads to various behavioral and biological alterations. OBJECTIVES: to describe the effects of alcohol on the CNS, identifying the signaling pathways that are modified and the biological effects resulting from its consumption. METHODS: a literature review was conducted and articles published in different languages over the last 15 years were retrieved. RESULTS: the studies reviewed describe the direct effect of alcohol on several neurotransmitter receptors (gamma-aminobutyric acid [GABA], glutamate, endocannabinoids AEA and 2-AG, among others), the indirect effect of alcohol on the limbic and opioid systems, and the effect on calcium and potassium channels and on proteins regulated by GABA in the hippocampus. DISCUSSION AND CONCLUSION: the multiple actions of alcohol on the CNS result in a general effect of psychomotor depression, difficulties in information storage and logical reasoning and motor incoordination, in addition to stimulating the reward system, a fact that may explain the development of addiction. Knowledge on the neuronal signaling pathways that are altered by alcohol allows the identification of effectors which could reduce its central action, thus, offering new therapeutic perspectives for the rehabilitation of alcohol addicts.

A review on alcohol: from the central action mechanism to chemical dependency / Uma revisão sobre o álcool: do mecanismo de ação central à dependência química

SummaryIntroduction:alcohol is a psychotropic depressant of the central nervous system (CNS) that promotes simultaneous changes in several neuronal pathways, exerting a profound neurological impact that leads to various behavioral and biological alterations.Objectives:to describe the effects of alcohol on the CNS, identifying the signaling pathways that are modified and the biological effects resulting from its consumption.Methods:a literature review was conducted and articles published in different languages over the last 15 years were retrieved.Results:the studies reviewed describe the direct effect of alcohol on several neurotransmitter receptors (gamma-aminobutyric acid [GABA], glutamate, endocannabinoids AEA and 2-AG, among others), the indirect effect of alcohol on the limbic and opioid systems, and the effect on calcium and potassium channels and on proteins regulated by GABA in the hippocampus.Discussion and conclusion:the multiple actions of alcohol on the CNS result in a general effect of psychomotor depression, difficulties in information storage and logical reasoning and motor incoordination, in addition to stimulating the reward system, a fact that may explain the development of addiction. Knowledge on the neuronal signaling pathways that are altered by alcohol allows the identification of effectors which could reduce its central action, thus, offering new therapeutic perspectives for the rehabilitation of alcohol addicts.

ResumoIntrodução:o álcool é uma substância psicotrópica depressora do sistema nervoso central (SNC), que promove alteração simultânea de inúmeras vias neuronais, gerando profundo impacto neurológico e traduzindo-se em diversas alterações biológicas e comportamentais.Objetivos:descrever as ações do álcool sobre o SNC, identificando as vias de sinalização modificadas e os efeitos biológicos gerados pelo seu consumo.Métodos:revisão bibliográfica, priorizando trabalhos multilinguísticos publicados nos últimos 15 anos.Resultados:são descritas ação direta do álcool em inúmeros receptores de neurotransmissores (ácido gama-aminobutírico – GABA, glutamato, endocanabinoides AEA e 2-AG, entre outros), ação indireta do álcool no sistema límbico e opioide, ação sobre canais de cálcio, potássio e proteínas reguladas por GABA no hipocampo, além de ações centrais mediadas pela deficiência de vitamina B1.Conclusão:a ação multifocal do álcool sobre o SNC resulta em efeito geral de depressão psicomotora, dificuldades no armazenamento de informações e no raciocínio lógico, incoordenação motora, além da estimulação do sistema de recompensa, o que pode explicar o desenvolvimento da dependência química. O conhecimento das vias de sinalização neuronais alteradas pelo álcool permite reconhecer a descrição de efetores que possam reduzir sua ação central e, assim, vislumbrar novas perspectivas terapêuticas para a reabilitação de adictos a essa substância.