Mitochondrial Defects in PBMCs of Children with Sepsis

Mitochondrial dysfunction has been implicated in the pathogenesis of organ injury related to the sepsis syndrome. This can be seen in the condition known as cytopathic hypoxia, wherein oxygen delivery is maintained, but the mitochondria are unable to efficiently convert this delivered oxygen to adenosine triphosphate (ATP) production. An energy deficit consequently arises. In adults, this diminished ability to produce adequate ATP has been demonstrated in peripheral blood mononuclear cells (PBMCs) of septic patients. Mitochondrial defects in PBMCs of septic children have not been previously described. Weiss et al sought to correlate defects in mitochondrial oxygen consumption and mitochondrial membrane potential in the PBMCs of children with septic shock of clinical severity. Twenty-eight children with septic shock were approached for consent. Ultimately, data from 13 patients were compared to those of 11 control subjects.

The authors found that mitochondrial dysfunction occurs in PBMCs from critically ill children with septic shock and multiple organ dysfunction syndrome. While this study has limitations related to the choice of cells studied, the timing of sampling and the numbers of patients, mitochondrial dysfunction in these patients is a significant finding that warrants further research.

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