Cerebrospinal fluid prostaglandins, interleukin 1 beta, and tumor necrosis factor in bacterial meningitis. Clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients
M. M. Mustafa, O. Ramilo, X. Saez-Llorens, K. D. Olsen, R. R. Magness and G. H. McCracken Jr
Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas.
Prostaglandins (PGs), interleukin 1 beta (IL-1 beta), and tumor necrosis
factor alpha (TNF alpha) are likely mediators of local inflammatory
reactions. We measured PGE2, PGI2, IL-1 beta, 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-1 beta, 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-1 beta, TNF, and lactate and
inversely correlated with glucose concentrations in the first CSF
specimens. The PGE2, PGI2, IL-1 beta, 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
TNF alpha concentrations in CSF2 specimens, those placebo-treated patients
with no detectable PGI2 or TNF alpha activity in CSF2 had a lower incidence
of neurological sequelae. Dexamethasone-treated patients had significantly
lower PGE2, IL-1 beta, 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.
