Urinary Hypoxanthine, Xanthine and Uric Acid Excretion in Newborn Infants With Perinatal Complications

Manzke, H; Dörner, Klaus; Grunitz, Juliane

doi:10.1111/j.1651-2227.1977.tb07977.x

Cited by 44 publications

(22 citation statements)

References 10 publications

(7 reference statements)

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“…The possibility of measuring the total excretion of purine metabolites, e.g., in the urine, might be expected to better fulfill the theoretical requirements of a quantitative variable of hypoxia. In a recent investigation, however, only 58% of infants with perinatal complications had an increased oxypurine excretion (13,14).…”

Section: Discussionmentioning

confidence: 94%

Hypoxanthine Concentration in Plasma during the First Two Hours after Birth in Normal and Asphyxiated Infants

Bratteby¹,

Swanström²

1982

Pediatr Res

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SummaryThe measurement of arterial plasma concentration of hypoxanthine in 16 healthy newborn infants showed a prominent increase after birth compared with the umbilical cord levels. Peak values were found 10-20 min after birth with a maximal value of 11.9 pmole/liter in the normal newborns. In five asphyxiated infants the postnatal pattern of hypoxanthine was the same as for normal infants but the increase was even more prominent. A mean peak value of 33.7 pmole/liter was noted in the asphyxiated infants. Our results indicate that the hypoxanthine concentration is influenced not only by the degree of hypoxia, but also by the peripheral circulation and the time interval between the hypoxic event and the blood sampling. It is concluded that hypoxanthine assay may be of clinical value for the detection of past hypoxia as a semiquantitative test. SpeculationIt is possible to differentiate a group of asphyxiated infants from normal infants by measurements of plasma hypoxanthine concentration. A new biochemical measure of perinatal hypoxia thus appears available. Knowledge about the change in hypoxanthine concentration is however of much greater value than that of a single plasma sample which may be &isleading.The theoretical connection between lack of oxygen, reduced cellular energy contents, and the catabolism of energy-rich phosphates (e.g., ATP, ADP) has been known for a long time. Until recently, however, the estimation of purine metabolites has not been used in clinical practice as a measure of hypoxia. With a micromethod for determination of the hypoxanthine concentration in plasma, Saugstad (18) found this metabolite to be a sensitive sign of hypoxia in experimental animals (20,21,22,23,24) and his preliminary clinical results also indicated a constant and slow decrease of this concentration after a period of fetal hypoxia. He therefore proposed that hypoxanthine measurements could be used for a retrograde estimation of past episodes of hypoxia in the newborn infant (19). In the umbilical cord plasma a hypoxanthine level of 11 pmole/liter was found to discriminate newborn infants with normal deliveries from infants with signs of intrauterine asphyxia (19). Lipp et al. (1 l), however, found that the hypoxanthine concentration in umbilical cord plasma from asphyxiated newborn infants overlapped in a rather broad range the values obtained from normal infants. This was true for both arterial and venous cord blood.In view of this discrepancy, the present study was undertaken in order to investigate the change in postnatal arterial hypoxanthine concentration in a number of normal and asphyxiated newborn infants who had been carefully monitored during delivery and in the early postnatal period. In some of these infants, the hypoxanthine concentration was also measured in venous cord blood and in the immediate neonatal period in blood samples obtained from the umbilical vein.

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Section: Discussionmentioning

confidence: 94%

Hypoxanthine Concentration in Plasma during the First Two Hours after Birth in Normal and Asphyxiated Infants

Bratteby¹,

Swanström²

1982

Pediatr Res

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“…High hypoxanthine values have been found in meconium stained amniotic fluid s well and this has been interpreted s a sign of intrauterine hypoxia [16]. Elevated oxypurine excretion in the urine by newborns after intrauterine hypoxia has been reported [12], although in another study on hypoxic newborns no such elevation in urine was found [10]. However, in the latter investigation, it is doubtful whether the investigators actually studied hypoxic babies, since these authors considered all babies with RDS to be hypoxic.…”

Section: Discussionmentioning

confidence: 99%

Plasma hypoxanthine levels in newbom infants: A specific indicator of hypoxia

Saugstad¹,

Gluck²

1982

Journal of Perinatal Medicine

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“…3). After this period the hypoxanthine concen- In newborn infants the urinary hypoxanthine excretion during the first 24 h of life is three to four times higher in babies suffering from intrauterine hypoxia compared with nonhypoxic babies (78). There was also a high correlation between the urinary hypoxanthine excretion and the hypoxanthine/creatinine ratio in the urine (r = 0.70) (79).…”

Section: Animal Studiesmentioning

confidence: 98%

Hypoxanthine as an Indicator of Hypoxia: Its Role in Health and Disease through Free Radical Production

Saugstad¹

1988

Pediatr Res

363

203

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Hypoxia is a common insult during the perinatal and neonatal period. New and better ways to evaluate hypoxia are needed. In 1975 we demonstrated high concentrations of the purine metabolite hypoxanthine in umbilical cord plasma after intrauterine hypoxia and proposed that hypoxanthine could be used as an indicator of hypoxia (1). Since then a large number of studies have been published dealing with different aspects of hypoxanthine in hypoxia. However, investigators in this field have encountered several methodologic problems: 1) Hypoxanthine leaks rapidly from erythrocytes (2, 3); if plasma is not separated promptly from red cells, falsely elevated plasma hypoxanthine concentrations will be found. 2) There are large variations in purine metabolism among species. 3) No clear definition of clinical hypoxia is available. Many authors do not distinguish between the terms hypoxemia and hypoxia, which adds to the confusion. We define tissue hypoxia as: "oxygen deficiency resulting in altered or interrupted energy metabolism" (4). It is important to be aware that hypoxia has two stages. In the first stage it is compensated because the cells are able to meet energy demands through anaerobic metabolism and other mechanisms. (We are not dealing with physiologic adaptation to hypoxia.) In the second stage of hypoxia or uncompensated hypoxia, energy demands are not met and cell injury ensues. At present there are no techniques for distinguishing between these two stages in clinical medicine, and such a distinction would be useful. Theoretically hypoxanthine should only be elevated in uncompensated hypoxia, while pH and lactate changes occur in compensated hypoxia. It seems, however, that hypoxanthine is also elevated to some extent in uncompensated hypoxia.Renewed interest in hypoxanthine developed when it was realized that hypoxanthine is a potential free radical generator (5, 6). Hypoxanthine seems to play a role in posthypoxic reoxygenation cell injury through oxygen radical production (7) and is therefore involved in the pathogenesis of a number of diseases. Hypoxanthine also modulates a number of other processes because it reacts with benzodiazepine receptors (8) and inhibits phosphodiesterase in the brain (9). Hypoxanthine inhibits the effect of several cytotoxic drugs and may therefore influence treatment with such drugs (10).Herein we summarize the extensive literature on hypoxanthine published during the last decade and try to answer the question: How useful in clinical medicine are hypoxanthine measurements in plasma and other body fluids? Is hypoxanthine a better marker of hypoxia than lactate or pH? Further, we discuss the significance of hypoxanthine as a potential oxygen radical generator and put forward a hypothesis for the pathogenesis of an "oxygen radical disease in neonatology". In hypoxia there is an accelerated breakdown of AMP to hypoxanthine. Figure 1 illustrates several important aspects of hypoxanthine metabolism in hypoxia. Normally about 90% of the hypoxanthine formed is reutilized through the sa...

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Urinary Hypoxanthine, Xanthine and Uric Acid Excretion in Newborn Infants With Perinatal Complications

Cited by 44 publications

References 10 publications

Hypoxanthine Concentration in Plasma during the First Two Hours after Birth in Normal and Asphyxiated Infants

Hypoxanthine Concentration in Plasma during the First Two Hours after Birth in Normal and Asphyxiated Infants

Plasma hypoxanthine levels in newbom infants: A specific indicator of hypoxia

Hypoxanthine as an Indicator of Hypoxia: Its Role in Health and Disease through Free Radical Production

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