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[Can glucose-6-phosphate dehydrogenase deficiency alone explain neonatal jaundice].

Several authors have insisted on the role of a glucose 6-phosphate deshydrogenase (G6PD) deficiency in the occurrence of neonatal jaundice which can be severe, leading to exchange transfusion. Considering the fact that haemolysis, occuring in deficient patients, is most of the time induced, our aim was to search if a neonatal hyperbilirubinemia could be explained by the sole G6PD deficiency or by extra "oxidant stress". Red blood cell G6PD activity of 289 newborn babies of African or Antillian origin was tested by a Tetrazolium linked method. 21 newborns were deficient. 8 female babies were heterozygous for G6PD deficiency. No neonatal jaundice was observed. With Bienzle and all., we can suppose that the "environment" takes an important part in the incidence of neonatal jaundice among G6PD deficient newborn of African or Antillian origin. However as triggering factors could be ignored, we think compulsary to search a G6PD deficiency in every neonatal jaundice necessitating an exchange-transfusion.

Africa

Red cell metabolism and severe neonatal jaundice in West Malaysia.

A study was carried out of 332 babies suffering from severe neonatal jaundice who were admitted to the General Hospital, Kuala Lumpar, Malaysia. Of the 332 neonates, 51 were premature and 281 were full-term babies, 178 (110 Chinese, 58 Malay, 9 Indian and 1 European-Pakistani) had bilirubin levels of 20 mg% or higher, requiring exchange blood transfusion. Of the Chinese neonates, 23 (20.9%) had G6PD deficiency, 9 (8.2%) had Hb Bart's and 2 (1.8%) had an abnormal haemoglobin, one Hb Q and one fetal variant. Among the Malay infants, 10 (17.2%) had G6PD deficiency, 7 (12.1%) had Hb Bart's and 10 (17.2%) had abnormal haemoglobins (four had Hb E trait, one had Hb K and Bart's in addition to Hb E, three had Hb CoSp with Hb Bart's, one had Hb Q and one Hb Tak). One of the nine Indian neonates had G6PD deficiency and one had Hb S trait. The one European-Pakistani baby was a carrier of Hb D Punjab. In addition to G6PD deficiency, abnormal haemoglobins seem to have contributed to the high incidence of severe neonatal jaundice in Malaysia. The mean activities of GP, GR and GR after stimulation with FAD were higher, while the mean activity of PK and mean level of reduced glutathione were lower than in normal cord bloods. The percent increase of GR after FAD stimulation was significantly lower; fewer in this group had increases above 20% than in normal cord blood. The possible significance of the findings is discussed.

Bilirubin

Prophylaxis of neonatal jaundice with maternal antipyrine treatment.

A randomised controlled trial of antipyrine (phenazone) in the prophylaxis of neonatal jaundice was completed in 48 women. Treatment of mothers from the 38th week of pregnancy reduced neonatal plasma-bilirubin concentrations on the 4th day after birth by an average of 44%. Prophylaxis of neonatal jaundice merits a wider trial.

Antipyrine

Factors influencing the incidence of neonatal jaundice.

A retrospective study of 12 461 single births confirmed an association between maternal oxytocin infusion and neonatal jaundice. The effect of oxytocin on jaundice was independent of gestational age at birth, sex, race, epidural anaesthesia, method of delivery, and birth weight, each of which was significantly associated with neonatal jaundice. The effect of oxytocin was, however, small, producing a calculated mean increase in peak plasma bilirubin concentration of 8.6 mumol/1 (0.5 mg/100 ml); this excess was independent of sex and less than the effect of the baby being born one week earlier.

Bilirubin

Neonatal jaundice.

This article discusses the production, transport, and excretion of bilirubin in the newborn period. The causes, significance, and treatment of unconjugated and conjugated hyperbilirubinemia are different; and because this is so, it is important to review the main causes and management of unconjugated hyperbilirubinemia. Conjugated hyperbilirubinemia in the newborn period could be either due to hepatocellular dysfunction or extrahepatic biliary obstruction. There are several recent advances in early differentiation and management of these two entities.

Adult

Factors affecting neonatal jaundice.

Plasma bilirubin was estimated on 690 term infants on about the 6th day of life. Perinatal factors were recorded and the results analysed. Hyperbilirubinaemia was defined as a level greater than 205 micromol/1 (12 mg/100 ml) and this was present in 20% of cases. Three factors--epidural analgesia, breast feeding, and poor weight recovery--showed highly significant associations with jaundice. The relative importance of these is discussed and compared with recent reports. Induction of labour, for reasons other than postmaturity, and a gestational age less than 39 weeks showed a slightly increased incidence of jaundice. There was no correlation with other factors tested including oxytocic drug administration. Despite the high incidence (20%) of hyperbilirubinaemia, only 2.5% infants needed treatment and none required exchange transfusion. Radical changes in obstetric management or infant feeding are not indicated.

Anesthesia, Epidural

Influence of simultaneous low amniotomy and oxytocin infusion and other maternal factors on neonatal jaundice: a prospective study.

In a prospective study of 196 consecutive single births a significant increase in serum bilirubin concentrations was found in infants born after low amniotomy induction and oxytocin infusion compared with those born spontaneously. This relationship was not dose-dependent and may have been associated with artificial interruption of pregnancy rather than the oxytocin itself. Infants delivered after spontaneous labour accelerated by oxytocin showed no such increase. The hormonal surge at the spontaneous onset of labour may affect fetal enzyme induction, but other factors, such as methods of infant feeding and oral contraceptive use, were found not to be significant.

Bilirubin