Abstract
It has been suggested that aspirin may be of benefit in treating sepsis and ARDS in view of its ability to block cyclo-oxygenase-1 (COX-1) and COX-2 activities; inhibit nuclear factor kappa B (NF-κB); enhance the production of endothelial nitric oxide (eNO) and lipoxin A4 (LXA4). Our previous studies revealed that plasma phospholipid content of arachidonic acid (AA) and eicosapentaenoic acid (EPA) is low in patients with sepsis. This implies that beneficial actions of aspirin in sepsis and ARDS is unlikely to be obtained in view of deficiency of AA and EPA, the precursors of LXA4 and resolvins respectively that are potent anti-inflammatory compounds and enhancers of eNO generation. In view of this, I propose that a combination of aspirin and AA and EPA (and possibly, docosahexaenoic acid, DHA) is likely to be superior in the management of sepsis and ARDS compared to aspirin alone. This suggestion is supported by the recent observation that trauma patients with uncomplicated recoveries had higher resolvin pathway gene expression and lower gene expression ratios of leukotriene: resolvin pathways.
Highlights
ARDS, sepsis and septic shock can lead to multiorgan dysfunction syndrome (MODS) that cause death among patients in non-coronary critical care units
I propose that a combination of aspirin and unsaturated fatty acids: arachidonic acid (AA, 20:4 n-6), eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3), the precursors of anti-inflammatory bioactive lipids lipoxin A4; resolvins; and protectins and maresins [38,39,40] is likely to be more suited and beneficial in managing sepsis and ARDS
We reported that patients with sepsis showed increased production of superoxide anion and hydrogen peroxide (H2O2) by their peripheral leukocytes; and enhanced levels of circulating lipid peroxides with a concomitant decrease in plasma phospholipid content of GLA, DGLA, AA of n-6 series and ALA, EPA and DHA of n-3 series [42]. These findings imply that decreased production of lipoxin A4 (LXA4), resolvins, protectins and maresins may occur due to a deficiency of their precursors (AA, EPA and DHA), which are potent anti-inflammatory bioactive lipids that may lead to perpetuation of the inflammatory process seen in sepsis and ARDS
Summary
ARDS (acute respiratory distress syndrome), sepsis and septic shock can lead to multiorgan dysfunction syndrome (MODS) that cause death among patients in non-coronary critical care units. These findings imply that decreased production of lipoxin A4 (LXA4), resolvins, protectins and maresins may occur due to a deficiency of their precursors (AA, EPA and DHA), which are potent anti-inflammatory bioactive lipids that may lead to perpetuation of the inflammatory process seen in sepsis and ARDS.
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