The first report on the levels of CoQ10 in human subjects with septic shock was published online on August 9, 2011 in the journal Critical Care. Sepsis is an inflammatory state resulting from the spread of infectious agents in the bloodstream. Sepsis and septic shock are a major cause of illness and mortality in the USA, with over 215,000 deaths occurring each year. The finding in this study that CoQ10 is low in sepsis opens the possibility for potential therapeutic intervention as CoQ10 can be administered exogenously.
Michael W Donnino, Michael N Cocchi, Justin D Salciccioli, Daniel Kim, Ali Naini, Catherine Buettner and Praveen Akuthota
Coenzyme Q10 levels are low and are associated with the inflammatory cascade in septic shock
Critical Care 2011; 15 (4): R189. [Epub ahead of print]
Mitochondrial dysfunction is associated with increased mortality in septic shock. Coenzyme Q10 (CoQ10) is a key cofactor in the mitochondrial respiratory chain but whether CoQ10 is depleted in septic shock remains unknown. Moreover, statin therapy may decrease CoQ10 levels but whether this occurs acutely remains unknown. We measured CoQ10 levels in septic shock patients enrolled in a randomized trial of simvastatin versus placebo.
Post-hoc analysis of a prospective randomized trial of simvastatin versus placebo in patients with septic shock (ClinicalTrials.gov ID: NCT00676897). Adult patients with suspected or confirmed infection and the need for vasopressor support were included in the initial trial. For the current analysis, blood specimens were analyzed for plasma CoQ10 and low-density lipoprotein levels. The relationship between CoQ10 levels and inflammatory and vascular endothelial biomarkers was assessed using Pearson or Spearman correlations.
28 samples from 14 patients were analyzed. CoQ10 levels were low with a median of 0.49 (IQR: 0.26 – 0.62) as compared to healthy control patients (CoQ10 = 0.95 umol/L +/- 0.29; p < 0.0001). Statin therapy had no effect on plasma CoQ10 levels over time (p = 0.13). There was a statistically significant relationship between CoQ10 level and vascular cell adhesion molecule (VCAM) (r2 = 0.2; p = 0.008), tumour necrosis factor- (r2 = 0.28; p=0.004), interleukin (IL)-8 (r2 = 0.21; p= 0.015), IL-10 (r2= 0.18; p=0.025), E-selectin (r2= 0.17; p=-0.03), IL-1ra (r2 =0.21; p=0.014), IL-6 (r2=0.17; p=0.029), and IL-2 (r2=0.23; p=0.009). Adjusting for low-density lipoprotein (LDL) levels there was a statistically significant inverse relationship between CoQ10 and VCAM (r2 = 0.24; p = 0.01; Figure 3) and IL-10 (r2 = 0.24; p = 0.02).
CoQ10 levels are significantly lower in patients with septic shock compared to healthy controls. CoQ10 is negatively associated with vascular endothelial markers and inflammatory molecules though this association diminishes when adjusting for LDL levels.
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