Erythrocyte and plasma selenium in children with acute inflammatory response.

OBJECTIVES: Plasma selenium may not reflect selenium status in critically ill patients because it transiently decreases inversely with the magnitude of the systemic inflammatory response. The decision to supplement selenium should ideally be based on laboratory measurements that reliably reflect selenium status. We hypothesized that erythrocyte selenium, unlike plasma selenium, is not affected by the systemic inflammatory response in critically ill children. METHODS: In a prospective study of 109 critically ill children, plasma and erythrocyte selenium concentrations were evaluated on admission, and plasma selenoprotein P was evaluated on days 1, 2, and 3 of the ICU stay. The main outcome was the effect of systemic inflammation on the erythrocyte and plasma selenium concentrations. The magnitude of the systemic inflammatory response was measured using serum C-reactive protein (CRP) and procalcitonin levels. The covariates were age, sex, anthropometric nutritional status, diagnosis of severe sepsis/septic shock, and clinical severity on admission. Multiple linear regression and generalized estimating equations were used for statistical analysis. RESULTS: Erythrocyte selenium levels were not influenced by the magnitude of the inflammatory response or by the patient's clinical severity. Procalcitonin (ß coefficient=-0.99; 95%CI: -1.64; -0.34, p = 0.003) and clinical severity (ß coefficient= -11.13; 95%CI: -21.6; -0.63), p = 0.038) on admission were associated with decreased plasma selenium concentrations. Erythrocyte selenium was associated with selenoprotein P in the first three days of ICU stay (ß coefficient=0.32; 95%CI: 0.20; 0.44, p < 0.001). CONCLUSION: Unlike plasma selenium, erythrocyte selenium does not change in children with an acute systemic inflammatory response and is associated with selenoprotein P concentrations. Erythrocyte selenium is probably a more reliable marker than plasma selenium for evaluating the selenium status in critically ill children.

Association of selenium status with endothelial activation during acute systemic inflammation in children.

BACKGROUND & AIMS: Evidence that selenium has a role in endothelial function comes mainly from experimental research, but few clinical studies have examined the pathophysiology of selenium in endothelial activation. We aimed to investigate whether there are associations between selenium status and the magnitude of endothelial activation and the severity of multiple organ dysfunction during the acute phase of systemic inflammatory response syndrome (SIRS) in children. METHODS: A prospective cohort study was carried out in 109 children with SIRS admitted to a pediatric ICU (PICU). Erythrocyte and plasma selenium were measured on admission and selenoprotein P and soluble plasma forms of the intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), sP-selectin, and endoCAM on days 1, 2 and 3 of hospitalization. Generalized estimating equations models were adjusted for clinical severity parameters, C-reactive protein, procalcitonin, and serum lactate. The effect of selenium status on organ dysfunction was defined by the Pediatric Logistic Organic Dysfunction (PELOD-2) during the PICU stay. RESULTS: Erythrocyte selenium was associated with sP-selectin and endoCAM, but not with ICAM-1 and VCAM-2. An increase of 10 µg/L in erythrocyte selenium resulted in increases of 43.2 ng/mL (p = 0.001) in sP-selectin and of 0.04 ng/mL (p < 0.001) in endoCAM. Erythrocyte selenium was also associated with a decrease in PELOD-2 (p = 0.015). Plasma selenium was not related to any of the outcomes. CONCLUSIONS: Erythrocyte selenium is associated with endothelial activation in the early phase of the systemic inflammatory response in children, and has a protective effect on multiple organ dysfunction during their PICU stay. Registered at: www.clinicaltrials.gov (NCT00708799).

Selenium and selenoproteins: from endothelial cytoprotection to clinical outcomes.

The role of the vascular endothelium in inflammation was demonstrated experimentally through biomarkers of endothelial dysfunction and cytoprotection. Selenium is a trace element essential for cell protection against oxidative lesions triggered by reactive oxygen species or inflammatory responses. Preclinical studies have demonstrated a relationship between adhesion molecules as biomarkers of endothelial dysfunction and selenoproteins as biomarkers of selenium status under conditions that mimic different diseases. Most studies in humans indicate an association between selenium deficiency and increased risk of morbidity and mortality, yet the pathophysiology of selenium in endothelial activation remains unknown. Here, we summarize selenium-dependent endothelial function evaluation techniques and focus on the role of selenium in endothelial cytoprotection according to current scientific knowledge. Most studies on the role of selenium in endothelial processes show selenium-dependent endothelial functions and explain how cells and tissues adapt to inflammatory insults. Taken together, these studies show an increase in adhesion molecules and a decrease in the expression of selenoproteins following a decreased exposure to selenium. Few clinical trials have enough methodological quality to be included in meta-analysis on the benefits of selenium supplementation. Furthermore, the methodology adopted in many studies does not consider the relevant findings on the pathophysiology of endothelial dysfunction. Preclinical studies should be more frequently integrated into clinical studies to provide clearer views on the role of selenium status in endothelial cytoprotection.

Níveis plasmáticos de vitamina A em crianças carentes com pneumonia na fase aguda e após recuperação / Plasma vitamin A levels in deprived children with pneumonia during the acute phase and after recovery

OBJETIVO: Comparar os níveis plasmáticos de retinol em crianças de baixo nível socioeconômico com pneumonia, antes e depois da resolução do processo infeccioso; investigar a associação entre os níveis plasmáticos de retinol, após a resolução da infecção, com algumas variáveis socioeconômicas, a condição nutricional e a gravidade da pneumonia. MÉTODOS: Estudo de coorte prospectivo desenvolvido com 40 crianças, hospitalizadas por pneumonia, na faixa etária de 6 meses a 5 anos. Foram avaliados o nível plasmático de retinol na fase aguda e após a resolução da infecção, a escolaridade do chefe da família, a renda per capita, o peso ao nascer, a condição nutricional, os níveis de hemoglobina e a gravidade da pneumonia. RESULTADOS: O valor médio de retinol plasmático após a resolução do processo infeccioso foi maior em relação à fase aguda da infecção (1,4±0,6 versus 1,7±0,6 æmol/l, p = 0,03). A freqüência de níveis inadequados de retinol (< 1,05 æmol/l) foi de 32,5 e 17,5 por cento na fase aguda e na resolução do processo infeccioso, respectivamente. Não se verificou relação estatisticamente significante entre a deficiência retinol e as variáveis clínico-epidemiológicas estudadas. A pneumonia mais grave foi observada em 30/40 (75 por cento) dos pacientes. Não houve diferença estatisticamente significante entre a inadequação dos níveis plasmáticos de retinol, após a resolução do processo infeccioso, com a gravidade da pneumonia (4/30 - 13,3 por cento versus 3/10 - 30,0 por cento, p = 0,34). CONCLUSAO: Os níveis plasmáticos de retinol foram mais altos após a resolução do processo infeccioso em relação à fase aguda, não havendo associação com as variáveis clínico-epidemiológicas estudadas.

Positivaçäo da pesquisa de Baar em lavado gastrico em criança com AIDS e tuberculose apos realizacao de puncao endobronquica via endoscopica / AFB detection in gastric secretion after endoscopic biopsy in a child with tuberculosis and AIDS

Os autores descrevem um caso de crianca com AIDS e doença pulmonar submetida a broncoscopia, como parte da investigaçäo diagnóstica de quadro pulmonar crônico. As pesquisas de BAAR realizadas previamente ao procedimento foram negativas, porém o paciente tornou-se bacilifero apos a realizaçäo do exame endoscopico. A negativaçäo da baciloscopia ocorreu somente apos 56 dias de tratamento