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Updated: Jun 6, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Serum amyloid A protein and hypoxic ischemic encephalopathy in the newborn
1Neonatology Division, The George Washington University & Children's National Medical Center, Washington, DC 20037, USA. haly@mfa.gw.edu
Objective:
Serum amyloid A (SAA) is an acute phase inflammatory marker that is closely associated with ischemic injuries. Its expression in neonatal hypoxic ischemic encephalopathy (HIE) has not been studied. To test the hypothesis that SAA is increased in neonatal HIE and its concentration correlates with the severity of encephalopathy.
Study Design:
We conducted a prospective case-control study on 54 full-term neonates; 27 cases with evidence of perinatal compromise and 27 healthy controls. Blood samples were collected from cases and controls at postnatal day 1 and day 7, and SAA was measured by ELISA.
Results:
SAA concentrations (μg ml(-1)) were significantly increased in cases when compared with controls at day 1 and at day 7 (P<0.001). SAA concentrations at day 1 were greater in cases who died when compared with those who survived, and correlated significantly with the severity of HIE (146.9 ± 56.4 vs 79.8 ± 24.7 vs 58.1 ± 21.5) in severe, moderate and mild HIE, respectively (P=0.001).
Conclusions:
The expression of SAA is increased in response to hypoxia ischemia of the neonate. The increased concentration correlates with the severity of encephalopathy and is associated with mortality. This is the first study of SAA in neonatal HIE.
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