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One of two late preterm twins at gestational age 36 weeks suffered idiopathiccerebral infarction. The first symptom was an apneic attack about 3 hours after birth.The lesion was extensive in the left middle cerebral artery region. Cord blood andearly postnatal serum levels of high mobility group box-1 (HMGB-1), histoneH3, andsyndecan-1 were measured simultaneously. All values of HMGB-1 remained within thereference value range. HMGB-1 and histoneH3 showed a very strong positive correlation(r=0.956). Syndecan-1 was detected but did not show a significant correlation witheither HMGB-1 or histoneH3. This twin was delivered by Caesarean section before thefirst labor pains, and it was suspected that the ischemia-reperfusion injury that occurs atbirth was minimal. Based on the serial changes of HMGB-1 in the early postnatal period,including in the umbilical cord blood, it is highly possible that the cerebral infarctionhad already occurred before birth. This case suggests that measurement of these threebiomarkers released into the blood by ischemic reperfusion injuries such as stroke maybe also useful for predicting these onsets.
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Neonatal cerebral infarction is a relatively rare central nervoussystem disorder that occurs in about 1 in 5000 neonates. The mostcommon cause is ischemic cerebral injury resulting from neonatalasphyxia but can also be idiopathic. Half of the infarctions developby the day 1, and few occur over the 3rd day of life. Most occur inthe middle cerebral artery region, most often on the left side [1-3]. Convulsions are the most common initial symptom, but thereare many non-specific symptoms such as decreased feeding abilityand apneic attacks. Treatment is mainly systemic managementand symptomatic treatment for convulsions. Currently, there areonly a few reported cases of the use of thrombomodulin, tissueplasminogen activator, and Edaravone (free radical scavenger),of which treatment method has been useful in adults [4], probablybecause of the many side effects for neonates. Neonatal cerebralinfarction is currently classified into six categories from theviewpoint of pathogenesis, and most of the idiopathic cerebralinfarctions belong to the category of ischemic cerebral infarction[1,2]. Similar cerebral ischemia and subsequent inflammation arepathological conditions of cerebral infarction in both newbornsand adults, and the indication for treatment depends on howmany hours have passed since the onset of cerebral infarction. Innewborns, infarct lesions may appear shortly after birth or mayhave already occurred before birth and may be diagnosed by thedetection of postnatal symptomsin the infant. Therefore, it is verydifficult to determine the onset of neonatal cerebral infarctioncompared to that of adults.We have confirmed and reported in a multicenter cohort studythat the effectiveness of brain hypothermia in neonatal asphyxiacan be judged by changes in the serum high mobility group box-1 (HMGB-1) concentration [5]. Furthermore, we observed theserial changes of HMGB-1 in the blood of infants who had alreadydeveloped fetal asphyxia and suffered severe sequelae even thoughbrain hypothermia was started within 6 hours after birth. We foundthat a long time had passed following the onset of ischemic lesionsand reported that postnatal brain hypothermia may be ineffectivefor such hypoxic ischemic encephalopathy within utero onset [6].This time we experienced a case of cerebral infarction in one of twotwins. We had the opportunity to simultaneously measure threebiomarkers, HMGB-1, histone H3, which is a nuclear protein similarto HMGB-1, and syndecan-1, which is present on the surface ofvascular endothelial cells and is thought to be released in the bloodduring angiopathy. As a result, we report a case in which the onsetof cerebral infarction was suspected to have occurred before birth. 2ff7e9595c
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