Cerebrospinal fluid prostaglandins, interleukin 1β, and tumor necrosis factor in bacterial meningitis. Clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients

M. M. Mustafa, O. Ramillo, X. Saez-Llorens, K. D. Olsen, R. R. Magness, G. H. McCracken

Research output: Contribution to journalArticle

109 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)883-887
Number of pages5
JournalAmerican Journal of Diseases of Children
Volume144
Issue number8
StatePublished - 1990

Fingerprint

Bacterial Meningitides
Interleukin-1
Dexamethasone
Epoprostenol
Prostaglandins
Cerebrospinal Fluid
Tumor Necrosis Factor-alpha
Placebos
Dinoprostone
Lactic Acid
Glucose
Incidence
Fever
Sodium

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Cerebrospinal fluid prostaglandins, interleukin 1β, and tumor necrosis factor in bacterial meningitis. Clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients. / Mustafa, M. M.; Ramillo, O.; Saez-Llorens, X.; Olsen, K. D.; Magness, R. R.; McCracken, G. H.

In: American Journal of Diseases of Children, Vol. 144, No. 8, 1990, p. 883-887.

Research output: Contribution to journalArticle

@article{7e6bcb1efe2e40f5a6e04106ed6053c9,
title = "Cerebrospinal fluid prostaglandins, interleukin 1β, and tumor necrosis factor in bacterial meningitis. Clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients",
abstract = "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.",
author = "Mustafa, {M. M.} and O. Ramillo and X. Saez-Llorens and Olsen, {K. D.} and Magness, {R. R.} and McCracken, {G. H.}",
year = "1990",
language = "English (US)",
volume = "144",
pages = "883--887",
journal = "JAMA Pediatrics",
issn = "2168-6203",
publisher = "American Medical Association",
number = "8",

}

TY - JOUR

T1 - Cerebrospinal fluid prostaglandins, interleukin 1β, and tumor necrosis factor in bacterial meningitis. Clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients

AU - Mustafa, M. M.

AU - Ramillo, O.

AU - Saez-Llorens, X.

AU - Olsen, K. D.

AU - Magness, R. R.

AU - McCracken, G. H.

PY - 1990

Y1 - 1990

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0025341682&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025341682&partnerID=8YFLogxK

M3 - Article

VL - 144

SP - 883

EP - 887

JO - JAMA Pediatrics

JF - JAMA Pediatrics

SN - 2168-6203

IS - 8

ER -