RESUMO
A 38-year-old male presented to the hospital with headache, fever, and meningeal signs. He had undergone a surgical review of a ventriculoperitoneal shunt system one month earlier. A head computed tomography scan showed hydrocephalus. His medical history included a human immunodeficiency virus infection identified four years before and resolved cryptococcal meningitis, which had necessitated the implantation of the shunt system. Ventricular cerebrospinal fluid (CSF) was obtained, which showed inflammation and, in culture, grew a Gram-negative bacillus identified as multidrug-resistant Klebsiella oxytoca. The shunt was removed and a ventricular drain was installed. Treatment with meropenem and amikacin was established without a response; the CSF white blood cell count continued to increase, with cultures remaining positive. The patient's clinical condition deteriorated to stupor. With informed consent, intraventricular (ITV) treatment with tigecycline was initiated at a dose of 5 mg every 24â¯h and, three days later, the CSF cultures were negativized. Tigecycline levels in the CSF were quantified by liquid chromatography with ultraviolet detection and showed peak concentrations achieved at two hours after the dose of between 178 and 310 µg/mL. After 11 days of treatment with ITV tigecycline and eight negative CSF cultures, a new CSF shunt was installed. During follow-up review 10 months later, the patient reported he was working. The dose of tigecycline used in this study produced levels 15 to 20 times the minimum inhibitory concentration of the bacteria for up to six hours with adequate tolerance.
Assuntos
Antibacterianos/uso terapêutico , Ventriculite Cerebral/tratamento farmacológico , Farmacorresistência Bacteriana Múltipla , Infecções por Klebsiella/tratamento farmacológico , Infecção da Ferida Cirúrgica/tratamento farmacológico , Tigeciclina/uso terapêutico , Derivação Ventriculoperitoneal , Adulto , Antibacterianos/líquido cefalorraquidiano , Fármacos Anti-HIV/uso terapêutico , Ventriculite Cerebral/complicações , Ventriculite Cerebral/diagnóstico , Ventriculite Cerebral/microbiologia , Combinação Efavirenz, Emtricitabina, Fumarato de Tenofovir Desoproxila/uso terapêutico , Infecções por HIV/complicações , Infecções por HIV/tratamento farmacológico , Humanos , Injeções Intraventriculares , Infecções por Klebsiella/complicações , Infecções por Klebsiella/diagnóstico , Infecções por Klebsiella/microbiologia , Klebsiella oxytoca/isolamento & purificação , Klebsiella oxytoca/fisiologia , Masculino , Testes de Sensibilidade Microbiana , Infecção da Ferida Cirúrgica/complicações , Infecção da Ferida Cirúrgica/diagnóstico , Infecção da Ferida Cirúrgica/microbiologia , Tigeciclina/líquido cefalorraquidianoRESUMO
Quinolinic acid (QUIN) striatal injection in rat reproduces the main neurochemical features of Huntington's disease (HD), including oxidative damage. In this study, we evaluated the effect of a copper (Cu) supplement in drinking water (90 ppm Cu, 28 days) on the QUIN-induced HD model in the rat. Copper exposure caused no signs of liver toxicity; however, it produced significant Cu accumulation in striatum. It is noteworthy that QUIN also caused increased striatal Cu content; when the supplement was administered to animals with QUIN-injury, an even higher metal striatal accumulation was observed. Cu pre-treatment preserved striatal gamma-aminobutyric acid (GABA) content, which was reduced by QUIN intrastriatal injection. Similarly, apomorphine-induced circling behavior was reduced in Cu-pretreated QUIN-damaged rats. Metal supplement in drinking water prevented both lipid peroxidation and reactive oxygen species (ROS) formation caused by QUIN in striatum. In Cu-treated groups, superoxide dismutase-1 (SOD1) activity showed a significant increase, while SOD2 activity was slightly enhanced. Although the pathophysiological role for higher Cu levels in patients with HD and in experimental models of the disease is not fully understood, results in the present study suggest that Cu oral intake stimulates anti-oxidant defenses, an effect that may be a potential factor for reducing the progression of HD.
Assuntos
Cobre/uso terapêutico , Doença de Huntington/tratamento farmacológico , Doença de Huntington/metabolismo , Animais , Apomorfina/toxicidade , Cobre/farmacologia , Modelos Animais de Doenças , Doença de Huntington/induzido quimicamente , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ácido Quinolínico/toxicidade , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/metabolismo , Ácido gama-Aminobutírico/metabolismoRESUMO
OBJECTIVE: The purpose of the study was to evaluate the effect of the pulsed electromagnetic fields (PEMF) and its possible modulation of the placebo effect in migraine. DESIGN: Placebo-controlled, randomized, double-blind, cross-over clinical trial. SETTING: Government third level hospital. INTERVENTIONS: Patients with migraine were included. PEMF were applied to the wrist with a bracelet. MAIN OUTCOME MEASURES: Frequency and intensity of the migraine attacks at baseline and during treatment were recorded. Also, we valuated the possible influence of gender and the presence of aura in the PEMF and placebo responses. RESULTS: Eighteen patients (fifteen women, 30±2 years old) were included. Migraine frequency and intensity was reduced with both PEMF and placebo to a similar extent in the whole population. However, in responders to placebo, migraine intensity was reduced to a median of 100% with the placebo and to 60% with the PEMF, while in non-responders there was only a slight effect of both treatments. Our results do not suggest an influence of gender or presence of aura in the outcomes. CONCLUSIONS: Treatment with PEMF may not alter either migraine intensity or frequency compared to baseline, but may reduce the response to placebo in migraine patients.
Assuntos
Campos Eletromagnéticos , Transtornos de Enxaqueca/terapia , Efeito Placebo , Placebos , Adulto , Estudos Cross-Over , Método Duplo-Cego , Feminino , Humanos , Masculino , Índice de Gravidade de Doença , Adulto JovemRESUMO
Dehydroepiandrosterone (DHEA) is synthesized in the brain and several studies have shown that this steroid is a modulator of synaptic transmission. The effect of DHEA, and its sulfate ester DHEAS, on glutamate and GABA neurotransmission has been extensively studied but some effects on other neurotransmitter systems, such as dopamine, serotonin and nitric oxide, have also been reported. This review summarizes studies showing the effect of DHEA and DHEAS on neurotransmitter systems at different levels (metabolism, release, reuptake, receptor activation), as well as the activation of voltage-gated ion channels and calcium homeostasis, showing the variety of effects that these steroids exert on those systems, allowing the discussion of its mechanisms of action and its relevance to psychiatric disorders.