PGE2 – metabolite levels in CSF correlate to HIE score and outcome after perinatal asphyxia

Authors


Correspondence

Eric Herlenius, MD, PhD, Department of Women's and Children's Health, Astrid Lindgren Children's Hospital Q2:07 Karolinska University Hospital, Karolinska Institutet, SE-171 76 Stockholm, Sweden.

Tel: +46 08 5177 0000 |

Fax: +46 08 5177 7353 |

Email: eric.herlenius@ki.se

Abstract

Aim

Acute anoxic exposure rapidly increases prostaglandin E2 (PGE2) production and release in neonatal mice brains. We hypothesize that PGE2 is released in human cerebrospinal fluid (CSF) during perinatal asphyxia and that it might be used as a biomarker for perinatal asphyxia.

Methods

In full-term infants with lumbar puncture performed within 72 h of birth (n = 35), CSF was analysed for prostaglandin E2 metabolite (PGEM) using an enzyme immunoassay. Term infants with suspected but unverified infections were used as controls (n = 11). Hypoxic–ischaemic encephalopathy (HIE) was classified as mild, moderate or severe (HIE I-III). Neurological assessment of surviving patients was performed at 18 months of age.

Results

Prostaglandin E2 metabolite levels correlated to a low Apgar score at 5 min (p < 0.01) and 10 min (p < 0.01), a low pH (p < 0.001) and HIE score (p < 0.05). The HIE-III cases (n = 7) had significantly higher PGEM levels compared with both controls and the HIE-I group (n = 8). Irrespective of HIE grade, patients with adverse or fatal outcome had higher PGEM values compared with controls and asphyxiated infants with normal outcome (p < 0.05).

Conclusions

PGE2 is released during anoxic events in newborn infants, and PGEM may be useful as a biomarker for estimating degree of insult and predicting long-term outcome after perinatal asphyxia.

Ancillary