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- [Show abstract] [Hide abstract] ABSTRACT: Severe malaria manifests as several overlapping syndromes with high mortality. Interaction of parasites with endothelial protein C receptors and high parasite biomass have recently been identified as key determinants of severe disease. However, gaps in our understanding of severe malaria might hinder translation of these findings into new therapies.
- [Show abstract] [Hide abstract] ABSTRACT: Severe malaria defines individuals at increased risk of death from their infection. Proposed pathogenic mechanisms include parasite sequestration, inflammation, and endothelial dysfunction. Severe malaria is not a single entity, manifesting with distinct syndromes such as severe anemia, severe respiratory distress or coma, each characterized by differences in epidemiology, underlying biology, and risk of death. The relative contribution of the various pathogenic mechanisms may differ between syndromes, and this is supported by accumulating evidence, which challenges sequestration as the initiating event. Here we propose that high parasite biomass is the common initiating feature, but subtle variations in the interaction between the host and parasite exist, and understanding these differences may be crucial to improve outcomes in patients with severe malaria.
- [Show abstract] [Hide abstract] ABSTRACT: Heat shock proteins are classified into six main families, of which HSP70 is the best studied. HSP70 is postulated to modulate the immune/inflammatory response in critical illness. Glutamine promotes HSP70 release, however, little is known about the relationship between glutamine and HSP70 in paediatric critical illness. We therefore aimed to describe plasma levels of HSP70, inflammatory mediators and glutamine in critically ill children. A clinical audit identified 143 children with severe meningococcal disease, 78 convalescent children, in addition to 35 healthy paediatric controls. Stored plasma was used to measure plasma concentrations of HSP70, inflammatory mediators and glutamine. HSP70 was significantly increased on admission (n = 143, mean 26.7 ng/ml; ±SD 79.95) compared with convalescence (n = 78, mean 3.16 ng/ml; ±SD 5.67). Glutamine levels were low (n = 132, mean 0.31 mmol/l; ±SD 0.13), which continued in convalescence (n = 65, mean 0.40 mmol/l; ±SD 0.14). Enteral glutamine provided only 28% of the recommendations. Glutamine was inversely correlated with length-of-stay (n = 98, r = -0.520, p < 0.001), ventilation (n = 98, r = -0.513, p < 0.001), lactate (n = 98, r = -0.41, p < 0.001) and CRP (n = 98, r = -0.51, p < 0.001). HSP70 was correlated with length-of-stay (n = 99, r = 0.30, p < 0.001), ventilation (n = 99, r = 0.31, p < 0.001), lactate (n = 99, r = 0.26, p < 0.001) and CRP (n = 99, r = 0.29, p < 0.001) and inflammatory mediators. There was no relationship between glutamine and HSP70 or inflammatory mediators. During acute illness HSP70/inflammatory mediators are significantly increased, and glutamine is significantly depleted. However, glutamine and HSP70 were not correlated. Enteral feeds only provided a small proportion of the ASPEN/ESPEN recommendations for glutamine.
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