Candidíase vulvovaginal : caracterização, tratamento, consequências da automedicação e o papel do farmacêutico na dispensação de medicamentos

As razões mais comuns pelas quais as mulheres procuram tratamento médico são as infecções ginecológicas. Dentre elas, a candidíase vulvovaginal (CVV) é considerada a segunda causa mais comum de infecção genital em mulheres em idade reprodutiva. O diagnóstico médico é muitas vezes realizado de forma empírica e o grande incômodo sentido pelas mulheres devido aos sintomas tem levado a prescrição precipitada de medicamentos e a prática da automedicação com medicamentos de venda livre. Este estudo teve como objetivo caracterizar a candidíase vulvovaginal discutindo as consequências da automedicação e o papel do farmacêutico na dispensação de medicamentos visando seu uso racional. Trata-se de uma revisão narrativa realizada por meio de busca nas bases de dados PubMed, Scopus e Google Acadêmico de onde foram selecionados um total de 17 estudos considerados relevantes para o tema. A partir dos estudos, concluiu-se que as falhas no diagnóstico e a automedicação podem estar envolvidas no aumento dos casos de candidíase vulvovaginal recorrente (CVVR) e, também, no aumento do número de casos de resistência aos agentes antifúngicos e que nesse contexto, o papel do farmacêutico é essencial, pois pode contribuir para diminuição nas taxas de resistência aos mesmos, e também para uma diminuição na incidência da CVVR impactando diretamente na melhora da qualidade de vida dessas mulheres.The most common reasons why women seek for medical treatment are the gynecological infections. Among them, the vulvovaginal candidiasis (VVC) is considered the second most common genital infection in women of reproductive age. The medical diagnosis is often performed in an empirical way and the discomfort felt by women due to the symptoms leads to a hasty prescription of medicine and also to the self-medication with over-the-counter medicines. This study aimed to characterize the VVC discussing the consequences of self-medication and the role of the pharmacists on medicine dispensing, aiming its rational use. This is a narrative review performed through researches on the PubMed, Scopus and Google Scholar data base, where 17 studies considered relevant for the topic were selected. From these studies it was concluded that the failures in diagnosis and the self-medication might be involved in the increase of cases of recurrent vulvovaginal candidiasis (RVVC) and also in the increase of resistance to antifungal agents. It was also concluded that in this context, the pharmacist’s role is essential and can contribute to the decrease of resistance to antifungal agent’s rates and also to the decrease of the incidence of RVVC, directly impacting on the improvement of the life quality of these women

Kynurenic acid restores Nrf2 levels and prevents quinolinic acid-induced toxicity in rat striatal slices

Kynurenic acid (KYNA) and quinolinic acid (QUIN) are metabolites produced in the degradation of tryptophan and have important neurological activities. KYNA/QUIN ratio changes are known to be associated with central nervous system disorders, such Alzheimer, Parkinson, and Huntington diseases. In the present study, we investigate the ability of KYNA in prevent the first events preceding QUIN-induced neurodegeneration in striatal slices of rat. We evaluated the protective effect of KYNA on oxidative status (reactive oxygen species production, antioxidant enzymes activities, lipid peroxidation, nitrite levels, protein and DNA damage, and iNOS immunocontent), mitochondrial function (mitochondrial mass, membrane potential, and respiratory chain enzymes), and Na+,K+-ATPase in striatal slices of rats treated with QUIN. Since QUIN alters the levels of Nrf2, we evaluated the influence of KYNA protection on this parameter. Striatal slices from 30-day-old Wistar rats were preincubated with KYNA (100 μM) for 15 min, followed by incubation with 100-μM QUIN for 30 min. Results showed that KYNA prevented the increase of ROS production caused by QUIN and restored antioxidant enzyme activities and the protein and lipid damage, as well as the Nrf2 levels. KYNA also prevented the effects of QUIN on mitochondrial mass and mitochondrial membrane potential, as well as the decrease in the activities of complex II, SDH, and Na+,K+-ATPase. We suggest that KYNA prevents changes in Nrf2 levels, oxidative imbalance, and mitochondrial dysfunction caused by QUIN in striatal slices. This study elucidates some of the protective effects of KYNA against the damage caused by QUIN toxicity

Hypoxanthine induces neuroenergetic impairment and cell death in striatum of young adult wistar rats

Hypoxanthine is the major purine involved in the salvage pathway of purines in the brain. High levels of hypoxanthine are characteristic of Lesch–Nyhan Disease. Since hypoxanthine is a purine closely related to ATP formation, the aim of this study was to investigate the effect of intrastriatal hypoxanthine administration on neuroenergetic parameters (pyruvate kinase, succinate dehydrogenase, complex II, cytochrome c oxidase, and ATP levels) and mitochondrial function (mitochondrial mass and membrane potential) in striatum of rats. We also evaluated the effect of cell death parameters (necrosis and apoptosis). Wistar rats of 60 days of life underwent stereotactic surgery and were divided into two groups: control (infusion of saline 0.9%) and hypoxanthine (10 μM). Intrastriatal hypoxanthine administration did not alter pyruvate kinase activity, but increased succinate dehydrogenase and complex II activities and diminished cytochrome c oxidase activity and immunocontent. Hypoxanthine injection decreased the percentage of cells with mitochondrial membrane label and increased mitochondrial membrane potential labeling. There was a decrease in the number of live cells and an increase in the number of apoptotic cells by caused hypoxanthine. Our findings show that intrastriatal hypoxanthine administration altered neuroenergetic parameters, and caused mitochondrial dysfunction and cell death by apoptosis, suggesting that these processes may be associated, at least in part, with neurological symptoms found in patients with Lesch–Nyhan Disease