Introduction
The use of low-dose corticosteroids in sepsis early stages is still debated. The association of LPS-LBP complexes to CD14 receptors and will interact with TLR4 to induce NF-κB as a signal and transcription of proinflammatory cytokines [1, 2]. Excessive production of inflammatory cytokines will cause activation of SIRS, especially in gut-associated lymphoid tissues [3], which induces metabolic changes leading to apoptosis network, MOF, septic shock and death [3–5]. Changes in apoptosis are mediated by caspases, including caspase-3 that acts as an effector caspase [6, 7]. Low-dose corticosteroids can inhibit the production of proinflammatory cytokines, production of inflammatory mediators, and lower adhesion of leukocytes to the endothelium [8].