INTRODUÇÃO: A epilepsia é um dos transtornos neurológicos mais comuns, sendo definido como uma condição de crises recorrentes espontâneas. Existe uma importante relação entre radicais livres e enzimas antioxidantes no fenômeno epiléptico, e as espécies reativas de oxigênio (EROs) têm sido implicadas na neurodegeneração induzida pelas crises. OBJETIVO: A presente revisão teve como objetivo investigar a relação existente entre o estresse oxidativo e a epilepsia, destacando o efeito da dieta cetogênica sob condições experimentais. MATERIAL E MÉTODOS: Procedeu-se a pesquisa em artigos científicos publicados nos Bancos de Dados Medline, PubMed, Periódicos CAPES, ScienceDirect e Scielo. As palavras-chave selecionadas para a pesquisa incluíram epilepsia, status epilepticus, pilocarpina, estresse oxidativo, espécies reativas de oxigênio, disfunção mitocondrial. RESULTADOS E DISCUSSÃO: Terapia dietética tem sido utilizada, como é o caso da dieta cetogênica (DC), a qual é rica em lipídeos e pobre em carboidratos e utilizada por mais de oito décadas para o tratamento de epilepsia refratária, principalmente em crianças. A DC modula a bionergética mitocondrial, diminui a formação de EROs, aumenta a capacidade antioxidante celular e ainda, previne alterações do DNA mitocondrial. CONCLUSÃO: Evidências de atuação da DC na disfunção mitocondrial, como ocorre na epilepsia, são muitas e demonstram claramente efeitos benéficos dessa terapêutica.
This study evaluated the effects of a ketogenic diet (KD) based on extra virgin coconut oil (Cocos nucifera L., VCO), on the treatment of epileptic rats. Two sets of experiments were conducted. First, male Wistar rats underwent induction of status epilepticus (SE) with the administration of pilocarpine intraperitoneally 21 animals reached spontaneous recurrent seizures (SRS) and were randomly allocated to the dietary regimens and video-monitored for 19 days. In the second experiment, 24 animals were randomized immediately after the induction of SE and followed for 67 days. Diets were as follows: Control (AIN-93G; 7% lipid), KetoTAGsoya (KD based on soybean oil; 69.79% lipid), and KetoTAGcoco (KD based on VCO; 69.79% lipid). There were no differences in the latency to the first crisis, total frequency, and duration of the SRS between groups in 2 experiments. The data suggest no effects of KD, with or without VCO, in rats with pilocarpine-induced epilepsy.
Introduction: Disturbances in intrauterine environment can have harmful effects on the fetus and pathological consequences persisting throughout adolescence and adulthood. Protein restriction during the prenatal period has a significant impact on growth and development of the central nervous system. Food restriction increases the risk of neurological disorders such as epilepsy. Objective: To relate the programming model by malnutrition and its implications in experimental epilepsy. Material and methods: There has been research papers published in the databases Medline, PubMed, CAPES journals, ScienceDirect and Scielo. The keywords selected for the study included epilepsy, Status Epilepticus, pilocarpine, malnutrition, programming. Results and discussion: Several studies in animal models or humans highlights the possible adverse effects of malnutrition at the onset of epileptic seizures. The vulnerability immunological, biochemical and electrolyte abnormalities and hypoglycemia may be the factors responsible for the intensification of the epileptogenic process in malnourished individuals. Conclusion: Malnutrition negatively changes the epileptogenic circuitry.
Introduction:
The established dose of chemotherapy is based on the values of the patient's body weight, where variations during treatment can increase the toxicity of chemotherapy, with the development of nephrotoxicity, among other toxicity profiles, as well as in cases of weight gain, patients may receive low doses and compromise the therapeutic response to the tumor.
Objective:
to evaluate weight gain and loss in cancer patients undergoing chemotherapy. Methods: Longitudinal analytical study with patients at the end of chemotherapy treatment of both genders. The type, location of the tumor and the antineoplastic agent used were collected from the medical records, as well as height and weight at the beginning of treatment. At the time of collection, anthropometric assessment was performed using body mass index, arm circumference, arm muscle circumference, triceps skinfold thickness and percentage of weight loss.
Results:
Among the patients included in the study, 47.5% had a weight gain of around 2.5 kg, while the remaining patients (52.5%) had a weight loss of around 2.8 kg. Of the patients who had GFR, 55.5% had severe PP, 33.4% had no significant loss and 11.1 had significant loss. In the current study, only 22% had a GFR <60ml/min/1.73m², but they would already need to readjust the medication calculation.
Conclusion:
It is important to evaluate body surface variations and also the GFR to adjust the dose of the antineoplastic agent and to prevent or minimize nephrotoxicity, as well as to reduce the risk of underdosing and inefficiency of the therapy.
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