Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Neuron-specific enolase (NSE) is a glycolytic enzyme present almost exclusively in neurons and neuroendocrine cells. NSE levels in cerebrospinal fluid (CSF) are assumed to be useful to estimate neuronal injury and clinical outcome of patients with serious clinical manifestations such as those observed in stroke, head injury, anoxic encephalopathy, encephalitis, brain metastasis, and status epilepticus. We compared levels of NSE in serum (sNSE) and in CSF (cNSE) among four groups: patients with meningitis (N = 11), patients with encephalic injuries associated with impairment of consciousness (ENC, N = 7), patients with neurocysticercosis (N = 25), and normal subjects (N = 8). Albumin was determined in serum and CSF samples, and the albumin quotient was used to estimate blood-brain barrier permeability. The Glasgow Coma Scale score was calculated at the time of lumbar puncture and the Glasgow Outcome Scale (GOS) score was calculated at the time of patient discharge or death. The ENC group had significantly higher cNSE (P = 0.01) and albumin quotient (P = 0.005), but not sNSE (P = 0.14), levels than the other groups (Kruskal-Wallis test). Patients with lower GOS scores had higher cNSE levels (P = 0.035) than patients with favorable outcomes. Our findings indicate that sNSE is not sensitive enough to detect neuronal damage, but cNSE seems to be reliable for assessing patients with considerable neurological insult and cases with adverse outcome. However, one should be cautious about estimating the severity of neurological status as well as outcome based exclusively on cNSE in a single patient.

Increased levels of glutamate in the central nervous system are associated with behavioral symptoms in experimental malaria

Cerebral malaria (CM) is a severe complication resulting from Plasmodium falciparum infection. This condition has been associated with cognitive, behavioral and motor dysfunctions, seizures and coma. The underlying mechanisms of CM are incompletely understood. Glutamate and other metabolites such as lactate have been implicated in its pathogenesis. In the present study, we investigated the involvement of glutamate in the behavioral symptoms of CM. Seventeen female C57BL/6 mice (20-25 g) aged 6-8 weeks were infected with P. berghei ANKA by the intraperitoneal route using a standardized inoculation of 10(6) parasitized red blood cells suspended in 0.2 mL PBS. Control animals (N = 17) received the same volume of PBS. Behavioral and neurological symptoms were analyzed by the SmithKline/Harwell/Imperial College/Royal Hospital/Phenotype Assessment (SHIRPA) battery. Glutamate release was measured in the cerebral cortex and cerebrospinal fluid of infected and control mice by fluorimetric assay. All functional categories of the SHIRPA battery were significantly altered in the infected mice at 6 days post-infection (dpi) (P ≤ 0.05). In parallel to CM symptoms, we found a significant increase in glutamate levels in the cerebral cortex (mean ± SEM; control: 11.62 ± 0.90 nmol/mg protein; infected at 3 dpi: 10.36 ± 1.17 nmol/mg protein; infected at 6 dpi: 26.65 ± 0.73 nmol/mg protein; with EGTA, control: 5.60 ± 1.92 nmol/mg protein; infected at 3 dpi: 6.24 ± 1.87 nmol/mg protein; infected at 6 dpi: 14.14 ± 0.84 nmol/mg protein) and in the cerebrospinal fluid (control: 128 ± 51.23 pmol/mg protein; infected: 301.4 ± 22.52 pmol/mg protein) of infected mice (P ≤ 0.05). These findings suggest a role of glutamate in the central nervous system dysfunction found in CM.

Fatores de risco para lesão renal aguda em pacientes com trauma grave e seus efeitos na mortalidade

Os estudos que relacionaram lesão renal aguda (LRA) e trauma surgiram durante a Segunda Guerra Mundial e, desde então, tem havido progressiva evolução dos cuidados para a prevenção da LRA. Entretanto, a determinação dos fatores de risco para o desenvolvimento de LRA pós-trauma permanece crucial e pode ajudar a reduzir esta complicação. OBJETIVO: Este estudo tem como objetivo identificar os fatores de risco para o desenvolvimento de LRA em pacientes com trauma grave e sua influência na mortalidade. Trata-se de um estudo retrospectivo com 75 pacientes incluídos por apresentarem trauma grave; seis foram excluídos por terem chegado ao hospital sem condições de ressuscitação. MÉTODO: As variáveis estudadas foram: idade, sexo, gravidade do trauma de acordo com Injury Severity Score (ISS) e Escala de Coma de Glasgow (ECG), mecanismo de trauma, pressão arterial média na admissão, reposição volêmica nas primeiras 24h, níveis séricos de creatinina, uso de antibióticos nefrotóxicos, tempo de internação, necessidade de internação em UTI e mortalidade. RESULTADOS: A prevalência de LRA em traumatizados graves foi de 17,3%, sendo que os fatores associados à IRA nessa amostra foram TCE, ECG < 10. A mortalidade, o tempo de internação e a necessidade de UTI foram significativamente maiores nos pacientes que desenvolveram LRA. CONCLUSÕES: A identificação desses fatores de risco é de suma importância para a formulação de estratégias de atendimento aos pacientes vítimas de trauma grave, visando à prevenção da lesão renal aguda e da elevada mortalidade.