It has been shown in experimental models of bacterial meningitis that bacterial cell-wall components produce an inflammatory response in the subarachnoid space, probably by stimulating the release of inflammatory cytokines, such as tumor necrosis factor, interleukin-1, and prostaglandins. Interleukin-1 increases the concentration of prostaglandin E2 and leukotriene B4, metabolites of arachidonic acid, which are potent mediators of inflammation. Steroidal and nonsteroidal anti-inflammatory agents decrease the formation of these metabolites and minimize the damage to the blood-brain barrier. There is also evidence that anti-inflammatory agents decrease cerebral edema in bacterial meningitis. The results of clinical trials in patients with bacterial meningitis demonstrate that dexamethasone can prevent sensorineural hearing loss and reduce mortality, without interfering with the antimicrobial action of antibiotics.
|Original language||English (US)|
|Number of pages||7|
|State||Published - Oct 8 1990|
ASJC Scopus subject areas
- Pharmacology (medical)