Relationship of uric acid concentrations and severe intraventricular hemorrhage/leukomalacia in the premature infant☆,☆☆,★,★★
Section snippets
Methods
Between January through September 1995, 58 premature infants <1250 gm birth weight admitted to the Neonatal Intensive Care Unit at Parkland Memorial Hospital were studied. Infants were excluded only if evidence of congenital abnormalities was found (n = 2).
Plasma was obtained for measurement of UA levels on the first and second postnatal days from laboratory samples that had previously been used for clinical analysis as part of the treatment of these infants. The Ectachem method (Johnson &
Patient Characteristics
The 58 infants had a birth weight of 865 ± 177 gm and a gestational age of 27 ± 2 weeks. Perinatal events included evidence of pregnancy-induced hypertension (n = 11), chorioamnionitis (n = 4), multiple gestation (n = 4), use of antenatal steroids (n = 20), cocaine exposure (n = 3), and intrauterine growth retardation (n = 1). The mode of delivery was vaginal (n = 24), nonemergent cesarean section (n = 30), or emergent cesarean section (n = 4). Delivery room resuscitation included oxygen only (n
Discussion
We have demonstrated a significant association between serum UA concentrations obtained in the first postnatal day and the development of severe IVH, cystic PVL, or both in the sick premature infant.
In humans UA is the end product of purine metabolism.3, 4 It is derived from either the increased turnover of purines or from the increased catabolism of tissue nucleic acids. Two isoenzymes, xanthine oxidase and dehydrogenase, degrade the purines, xanthine, and hypoxanthine to UA. Xanthine
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Cited by (51)
Periventricular- intraventricular hemorrhage in the premature infant- A historical perspective
2022, Seminars in PerinatologyCitation Excerpt :Since both the GM and the periventricular white matter represent border zone regions, the risk for ischemic injury is increased during periods of systemic hypotension, particularly in the face of a pressure passive cerebral circulation.16 Indeed, elevated hypoxanthine and uric acid levels (perhaps as markers of reperfusion injury) have been observed on the first postnatal day in infants who subsequently developed white matter injury.18,19 Cerebral autoregulation is the intrinsic ability of the cerebral blood vessels to maintain relatively constant CBF over a range of systemic blood pressures.
Cerebral White Matter Injury: Pathogenesis
2018, Volpe's Neurology of the NewbornIntraventricular Hemorrhage and White Matter Injury in the Preterm Infant
2018, Neurology: Neonatology Questions and ControversiesHypoxic-Ischemic Injury in the Term Infant
2018, Volpe's Neurology of the NewbornPreterm Intraventricular Hemorrhage/Posthemorrhagic Hydrocephalus
2018, Volpe's Neurology of the NewbornPathogenesis of Germinal Matrix Hemorrhage
2017, Fetal and Neonatal Physiology, 2-Volume Set
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From the Department of Pediatrics, UT Southwestern Medical Center, Dallas, Texas.
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Supported by GCRC MO1-RR00633.
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Reprint requests: Jeffrey M. Perlman, MB, Department of Pediatrics, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235-9063.
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0022-3476/98/$5.00 + 0 9/21/84994