Relationship of uric acid concentrations and severe intraventricular hemorrhage/leukomalacia in the premature infant,☆☆,,★★

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Abstract

The purine metabolite hypoxanthine accumulates with hypoxia ischemia and with reperfusion is converted to uric acid (UA). We hypothesized that elevated UA concentration is a marker of previous hypoxia ischemia and would identify infants at greatest risk for having subsequent intraventricular hemorrhage (IVH)/periventricular leukomalacia (PVL). We determined the relationship between UA concentrations in the first postnatal day and the development of severe IVH, PVL, or both in 58 infants of birth weight 865 ± 177 gm and gestational age 27 ± 2 weeks. Severe IVH developed in 10 (17%) infants and PVL in 3 (5.1%) infants. UA concentrations on day 1 (obtained at 16 ± 4 hours) were 7.9 ± 2.8 mg/dl and increased to 9.5 ± 2.58 mg/dl on day 2. UA concentrations on day 1 were higher in infants with severe IVH/PVL versus those in infants with neither condition: 10.2 vs 7.3 mg/dl (p = 0.005). Infants with hyperkalemia on the second postnatal day had higher UA concentrations on the first day versus infants with normal potassium levels: 11.7 ± 2 mg/dl versus 6.8 ± 1.8 mg/dl (p < 0.0005). Infants with severe IVH/PVL had higher potassium levels on day 2 versus infants with neither condition: 11.9 vs 6.9 mg/dl (p < 0.048). By univariate analysis UA concentrations were significantly related to gestational age (p = 0.005) and birth weight (p = 0.03). Only UA concentration (p = 0.004) and gestational age (p = 0.02) were related to IVH/PVL. By multivariate analysis UA remained significantly related to IVH/PVL even when adjusted for other clinical variables, with an odds ratio estimate of 1.63 (95% confidence interval 1.16 to 2.31). In conclusion, higher UA concentrations on the first postnatal day were associated with the subsequent development of severe IVH/PVL and with subsequent hyperkalemia. Elevated UA concentrations in the first postnatal day may help to identify a subset of premature infants at greatest risk for having subsequent hemorrhagic ischemic injury. (J Pediatr 1998;132:436-9)

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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From the Department of Pediatrics, UT Southwestern Medical Center, Dallas, Texas.

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Supported by GCRC MO1-RR00633.

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

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