Cerebrospinal Fluid Prostaglandins, Interleukin 1β, and Tumor Necrosis Factor in Bacterial Meningitis: Clinical and Laboratory Correlations in Placebo-Treated and Dexamethasone-Treated Patients

• Prostaglandins (PGs), interleukin 1β (IL-1β), and tumor necrosis factor α (TNFα) are likely mediators of local inflammatory reactions. We measured PGE₂, PGI₂, IL-1β, and TNF concentrations in paired cerebrospinal fluid (CSF) samples (on admission, CSF₁, and 18 to 30 hours later, CSF₂) from 80 infants and children with bacterial meningitis. Forty patients received dexamethasone sodium (0.6 mg/kg per day in four intravenous doses) and 40 received an intravenous saline placebo. In CSF₁, PGE₂, PGI₂, IL-1β, and TNF were detected in 90%, 56%, 98%, and 71% of specimens with mean (± SEM) concentrations of 462±65, 377±62, 1266±242, and 799±227 pg/mL, respectively. Concentrations of PGE₂ correlated significantly with PGI₂, IL-1β, TNF, and lactate and inversely correlated with glucose concentrations in the first CSF specimens. The PGE₂, PGI₂, IL-1β, and TNF were still detected in 40%, 18%, 97%, and 60%, respectively, of second CSF specimens obtained from placebo-treated patients. Compared with patients who had detectable PGI₂ or TNFα concentrations in CSF₂ specimens, those placebo-treated patients with no detectable PGI₂ or TNFα activity in CSF₂ had a lower incidence of neurological sequelae. Dexamethasone-treated patients had significantly lower PGE₂, IL-1β, and lactate concentrations and higher glucose concentrations in CSF 18 to 30 hours later, shorter duration of fever, and a lower incidence of neurological sequelae than did placebo-treated patients.