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Clinical and Laboratory Correlations in Placebo-Treated and Dexamethasone-Treated Patients

Mahmoud M. Mustafa, MD; Octavio Ramilo, MD; Xavier Sáez Llorens, MD; Kurt D. Olsen; Ronald R. Magness, PhD; George H. McCracken, Jr, MD

Am J Dis Child. 1990;144(8):883-887.

Abstract
• Prostaglandins (PGs), interleukin 1β (IL-1β), and tumor necrosis factor (TNF) 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 TNF concentrations in CSF₂ specimens, those placebo-treated patients with no detectable PGI₂ or TNF 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.

(AJDC. 1990;144:883-887)

Author Affiliations
From the Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas.

Footnotes
Accepted for publication December 28, 1989.

Reprints not available.

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