Background. According to the Consensus 2010 of the International Liaison Committee on Resuscitation (ILCOR), children with moderate to severe hypoxic-ischemic encephalopathy (HIE) should receive brain hypothermic therapy (BHT) after successful resuscitation. Elevated high mobility group box 1 (HMGB1) in the blood at the early stage of brain ischemia-reperfusion injury has been suggested to be involved in the release of various inflammatory cytokines. Methods. In total, 21 neonates plasma HMGB1 concentration was measured. These neonates included 8 with HIE in whom BHT was indicated, 5 controls diagnosed as having HIE but who were not suitable candidates for BHT, and 8 normal controls. Results. The umbilical artery HMGB1 (UA-HMGB1) level before undergoing BHT significantly exceeded reference values. The UA-HMGB1 level in the BHT (−) group did not differ significantly from reference values, but was significantly increased 24 hours after birth. Repeated measure ANOVA showed a significant difference in time course changes between the BHT (+) and BHT (−) groups (P = 0.0002). Conclusions. This study demonstrated hypothermic therapy to significantly decrease HMGB1. Furthermore, HMGB1 is a useful index of the inhibition of early stage inflammation.
We report the case of a baby with low birthweight born by emergency caesarean section at 33 weeks 2 days' gestation due to placental abruption. High-mobility group box-1 (HMGB-1) and interleukin-17 concentration in the umbilical cord blood were high at 55.7 ng/mL and 50.7 pg/mL, respectively. On immunostaining of umbilical cord and amniotic epithelium, HMGB-1 was identified in the nuclei of vascular endothelial cells and cytoplasm of the surrounding cells in the umbilical cord. This suggests that, in the present case of placental abruption and subsequent ischemic placenta and fetus, the high level of HMGB-1 observed was due to the release of HMGB-1 into the umbilical cord blood from the vascular endothelial cells of the umbilical cord.
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