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1.
Rev. colomb. gastroenterol ; 36(4): 485-493, oct.-dic. 2021. tab
Artigo em Inglês, Espanhol | LILACS | ID: biblio-1360973

RESUMO

Resumen El nuevo coronavirus del síndrome respiratorio agudo grave de tipo 2 (SARS-CoV-2), virus que se ha expandido por todo el mundo, produce una infección respiratoria aguda capaz de producir la muerte; sin embargo, el daño en otros órganos también es frecuente. Diversos estudios han evidenciado alteraciones en pruebas de lesión hepáticas, las cuales se han asociado con enfermedad grave y mayor estancia hospitalaria; así mismo, en la infección por el virus en pacientes con enfermedad hepática preexistente se observó una elevación significativa de las aminotransferasas durante el curso de la enfermedad y mayor riesgo de enfermedad grave. La explicación fisiopatológica de la afectación hepática en estos pacientes abarca el efecto citopático directo producido por la unión del virus a la enzima convertidora de la angiotensina II (ECA-II) a los hepatocitos y colangiocitos, una respuesta inmunitaria desproporcionada y, en algunos casos, la hepatotoxicidad por medicamentos.


Abstract The new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a virus that has spread around the world, causes an acute respiratory infection and it may also cause death. The damage that can cause in other organs is frequent. Many studies had also shown alterations in liver function tests, that are then related to serious illness and with hospitalization requirements. Moreover, in patients infected with the virus that had underlying liver disease, a significant increase in the level of aminotransferases was observed in the course of the disease. A greater risk of serious illness was also detected. The pathophysiological explanation of liver injury in those patients covers the direct cytopathic effect produced by binding the virus, the angiotensin-converting enzyme (ACE2) to the hepatocytes and the cholangiocytes, excessive immune response, and in some cases, drug-induced hepatotoxicity.


Assuntos
Humanos , Hepatócitos , SARS-CoV-2 , Infecções , Literatura , Fígado , Remoção , Enzimas , Hepatopatias
3.
J Neurosci Rural Pract ; 9(4): 478-486, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30271037

RESUMO

BACKGROUND AND OBJECTIVES: Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, used for the management of hypercholesterolemia and related atherosclerotic diseases. Several studies have indicated the neuroprotective effects of statins on several neuropathological conditions. However, the role of these medications in epilepsy is still unclear. The purpose is to evaluate and summarize the level of evidence on the efficacy of statins in neuronal hyperexcitability and the neuroinflammatory processes of epilepsy. METHODS: A systematic review was performed. Eligibility Criteria: This review involved studies conducted in humans and nonhuman experimental models, covering the use of an inhibitor of HMG-CoA reductase, alone or accompanied by another medication, in epilepsy. Information Sources: A systematic literature search was performed in PubMed, Embase, Ebsco Host, Scopus, Science Direct, Medline, and LILACS. Risk of Bias: It was evaluated with the Newcastle-Ottawa Scale and the experimental studies were evaluated using the GRADE tool. RESULTS: Twenty articles of the 183 evaluated were included. Sixteen studies were conducted in animal models and four studies in humans. Most studies in mice reported a reduction in epileptiform activity and reduction in systemic inflammation with the treatment of statins, potentially influencing epilepsy control. Few studies in humans were performed in the geriatric population with variable results (neuroinflammation, seizure prevention, cell death, prevention of kindling, increase in convulsive threshold, increase in latency, decrease in frequency of crisis, and reduction in mortality) related to reduction in the rate of hospitalizations, mortality, and prevention of epilepsy. Studies in mice found a decrease in interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor alpha and an increase in IL-10 and endothelial nitric oxide synthase. CONCLUSIONS: The possible antiepileptic mechanism of statins may be related to the reduction in neuroinflammation mediated by a decrease in pro-inflammatory cytokines and action in the nitrergic system. Further studies evaluating the impact of statins on seizure control are necessary.

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