Avaliação do atendimento laboratorial a sintomáticos respiratórios para tuberculose que procuraram serviços de saúde em Canoas, Rio Grande do Sul, Brasil, 2012

OBJETIVO: descrever o tempo decorrido entre a identificação do sintomático respiratório para tuberculose e a liberação do resultado laboratorial, bem como entre a obtenção do resultado e o início do tratamento. MÉTODOS: estudo descritivo, com dados de casos suspeitos de tuberculose atendidos em serviços públicos de saúde no município de Canoas-RS, Brasil, em 2012. RESULTADOS: foram examinados 1.138 pacientes, com positividade de 7,47%; as medianas de tempo (i) entre identificação do paciente e entrada da amostra de escarro no laboratório e de (ii) processamento do exame foram de 2 (intervalo interquartílico [IIQ] 1-3) e 3 dias (IIQ 1-4), respectivamente, para pacientes com resultado negativo; para pacientes com resultado positivo, esses tempos foram de 2 (IIQ 1-3) e 2,5 dias (IIQ 1-4); entre a liberação do resultado e início do tratamento, transcorreram 3 dias (IIQ 0-5). CONCLUSÃO: os tempos avaliados foram considerados longos em comparação ao preconizado pelo Ministério da Saúde

Crosstalk among disrupted glutamatergic and cholinergic homeostasis and inflammatory response in mechanisms elicited by proline in astrocytes

Hyperprolinemias are inherited disorder of proline (Pro) metabolism. Patients affected may present neurological manifestations, but the mechanisms of neural excitotoxicity elicited by hyperprolinemia are far from being understood. Considering that the astrocytes are important players in neurological disorders, the aim of the present work was to study the effects 1 mM Pro on glutamatergic and inflammatory parameters in cultured astrocytes from cerebral cortex of rats, exploring some molecular mechanisms underlying the disrupted homeostasis of astrocytes exposed to this toxic Pro concentration. We showed that cortical astrocytes of rats exposed to 1 mM Pro presented significantly elevated extracellular glutamate and glutamine levels, suggesting glutamate excitotoxicity. The excess of glutamate elicited by Pro together with increased glutamate uptake and upregulated glutamine synthetase (GS) activity supported misregulated glutamate homeostasis in astrocytic cells. High Pro levels also induced production/release of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. We also evidenced misregulation of cholinergic anti-inflammatory system with increased acetylcholinesterase (AChE) activity and decreased acetylcholine (ACh) levels, contributing to the inflammatory status in Pro-treated astrocytes. Our findings highlighted a crosstalk among disrupted glutamate homeostasis, cholinergic mechanisms, and inflammatory cytokines, since ionotropic (DL-AP5 and CNQX) and metabotropic (MCPG and MPEP) glutamate antagonists were able to restore the extracellular glutamate and glutamine levels; downregulate TNFα and IL6 production/release, modulate GS and AChE activities; and restore ACh levels. Otherwise, the non-steroidal anti-inflammatory drugs nimesulide, acetylsalicylic acid, ibuprofen, and diclofenac sodium decreased the extracellular glutamate and glutamine levels, downregulated GS and AChE activities, and restored ACh levels in Pro-treated astrocytes. Altogether, our results evidence that the vulnerability of metabolic homeostasis in cortical astrocytes might have important implications in the neurotoxicity of Pro