Sepsis, or SIRS, is a maladaptive reaction to severe infection in which a variety of inflammatory mediators are released. Some of these mediators are bacterial metabolic products, while others are cytokines produced by humans during infection or other inflammatory disease. These mediators can induce failure of several organ systems. Cardiac function can be suppressed; acute respiratory distress syndrome can occur; renal failure is common; and disseminated intravascular coagulation can occur.

Through their ability to cause cell lysis, antibiotics such as the p-lactams or aminoglycosides may increase the release of bacterial inflammatory mediators (e.g., gram-negative bacillary endotoxin). Antibiotics also may induce the release of endogenous cytokines, such as interleukin (IL) 1-p, IL-6, and tumor necrosis factor (TNF-a) from monocytes and IL-4 and IFN-7 from lymphocytes. These cytokines are important in inflammatory and immunological responses and may contribute to the development of SIRS. Alternatively, these cytokines also may enhance immune function and enhance antimicrobial activity. Although many drugs have been examined for their ability to reverse SIRS, no clinical studies of interventions in sepsis have yet been shown to significantly lessen mortality.

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