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and interleukin-1
concentrations on outcome of
full term infants with hypoxic-ischaemic encephalopathy
inb
a Akdeniz University Medical School
Department of Pediatrics, Division of Neonatology,
Antalya Turkey, b Division of Immunology, c Department of Biostatistics
Correspondence to: Dr Nihal Oygür.
Accepted 10 May 1998
AIM
To determine the predictive value of plasma
and cerebrospinal fluid (CSF) tumour necrosis factor-
(TNF-
) and
interleukin-1
(IL-1
) concentrations on the outcome of
hypoxic-ischaemic encephalopathy (HIE) in full term infants.
METHODS
Thirty term infants with HIE were included
in the study. HIE was classified according to the criteria of Sarnat
and Sarnat. Blood and CSF were obtained within the first 24 hours of
life and stored until assay. Five infants died soon after hypoxic
insult. Neurological examinations and Denver Developmental Screening
Test (DDST) were performed at 12 months in the survivors.
RESULTS
At the age of 12 months neurological
examination and DDST showed that 11 infants were normal; 14 had
abnormal neurological findings and/or an abnormal DDST result. Eleven
normal infants were classified as group 1 and 19 infants (14 with
abnormal neurological findings and/or an abnormal DDST and five who
died) as group 2. CSF IL-1
and TNF-
concentrations in group 2 were significantly higher than those in group 1. Plasma IL-1
and
TNF-
concentrations were not significantly different between the two
groups. IL-1
, but not TNF-
concentrations, in group 2 were even
higher than those in group 1, although non-survivors were excluded from
group 2. When the patients were evaluated according to the stages of Sarnat, the difference in the three groups was again significant. Patients whose CSF samples were taken within 6 hours of the hypoxic insult had higher IL-1
and TNF-
concentrations than the patients whose samples were taken after 6 hours.
CONCLUSIONS
Both cytokines probably contribute to
the damage sustained by the central nervous system after hypoxic
insult. IL-1
seems to be a better predictor of HIE than TNF-
.
;
interleukin-1
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