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Pathophysiology of Pediatric Multiple Organ Dysfunction Syndrome #MMPMID28248832
Pediatr Crit Care Med 2017[Mar]; 18 (3 Suppl 1): S32-45 PMID28248832show ga
Objective: To describe the pathophysiology associated with multiple organ dysfunction syndrome (MODS) in children. Data Sources: Literature review, research data, and expert opinion Study Selection: Not applicable Data Extraction: Moderated by an experienced expert from the field, pathophysiological processes associated with MODS in children were described, discussed and debated with a focus on identifying knowledge gaps and research priorities. Data Synthesis: Summary of presentations and discussion supported and supplemented by relevant literature. Conclusions: Experiment modeling suggests that persistent macrophage activation may be a pathophysiologic basis for MODS. Children with MODS have 1) reduced cytochrome P450 metabolism inversely proportional to inflammation, 2) increased circulating damage associated molecular pattern molecules (DAMPS) from injured tissues, 3) increased circulating pathogen associated molecular pattern molecules (PAMPS) from infection or endogenous microbiome, and 4) cytokine driven epithelial, endothelial, mitochondrial, and immune cell dysfunction. Cytochrome P450s metabolize endogenous compounds and xenobiotics, many of which ameliorate inflammation, whereas DAMPS and PAMPS alone and together amplify the cytokine production leading to the inflammatory MODS response. Genetic and environmental factors can impede inflammation resolution in children with a spectrum of MODS pathobiology phenotypes. Thrombocytopenia associated MODS patients have extensive endothelial activation and thrombotic microangiopathy with associated oligogenic deficiencies in inhibitory complement and ADAMTS13. Sequential MODS patients have sfasL-fas mediated hepatic failure with associated oligogenic deficiencies in perforin and granzyme signaling. Immune paralysis associated MODS patients have impaired ability to resolve infection, and have associated environmental causes of lymphocyte apoptosis. These inflammation phenotypes can lead to macrophage activation syndrome. Resolution of MODS requires elimination of the source of inflammation. Full recovery of organ functions is noted six to eighteen weeks later when epithelial, endothelial, mitochondrial, and immune cell regeneration and reprogramming is completed.
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Pediatr+Crit+Care+Med 2017 ; 18 (3 Suppl 1): S32-45
