Phototherapy for neonatal hyperbilirubinemia in mature newborn infants with erythrocyte G-6-PD deficiency

Meloni, T; Costa, Sinfarosa; Dore, Angelo; Cutillo, S

doi:10.1016/s0022-3476(74)80470-1

Cited by 14 publications

(4 citation statements)

References 4 publications

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“…Photo-oxidation makes a minor contribution to the decline in bilirubin levels, as it is a slow process [46]. Randomized trials have demonstrated that phototherapy reduces the rate of exchange in infants with haemolysis due to ABO incompatibility or glucose-6-phosphate dehydrogenase de®ciency [31], but such trials have not been performed in infants with Rh disease. The colour of the light used aects the ecacy of phototherapy; bilirubin is a yellow pigment and absorbs violet, blue and to certain extent green light [15].…”

Section: Phototherapymentioning

confidence: 99%

Rhesus disease: postnatal management and outcome

Greenough¹

1999

European Journal of Pediatrics

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The incidence of rhesus haemolytic disease has been markedly reduced. Affected infants who have had intrauterine transfusions suffer a late hyporegenerative anaemia. Postnatal haemolysis and hence treatment for hyperbilirubinaemia is less commonly needed. Optimal phototherapy reduces the need for postnatal exchange transfusions, but data on the efficacy of inhibitors of bilirubin production such as haem oxygenase inhibitors or immunoglobulin are less secure. Even hydropic infants have less than 20% mortality and bilirubin encephalopathy is uncommon. There is, however, very limited information on the long-term outcome of infants with rhesus haemolytic disease. Multicentre collaboration is required to test strategies to improve the management of affected individuals further and to provide meaningful data on their prognosis.

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Section: Phototherapymentioning

confidence: 99%

Rhesus disease: postnatal management and outcome

Greenough¹

1999

European Journal of Pediatrics

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“…Only as far as favism is concerned have Siniscalco et al [8] found a lower incidence and a lesser severity of hemolytic crises in G-6-PD deficient carriers of the fl-thalassemic trait. In our opinion, however, it is unlikely that there is any connection between favism and neonatal hyperbilirubinemia due to G-6-PD deficiency since our experience of the latter indicates that it is not of an overt hemolytic nature [5,9,10].…”

Section: Discussionmentioning

confidence: 66%

β-Thalassemia trait and hyperbilirubinemia in G-6-PD deficient newborn infants

Meloni

Gallisai

et al. 1980

Eur J Pediatr

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Hb A2 was determined in 50 subjects with erythrocyte G-6-PD deficiency who presented with hyperbilirubinemia in the neonatal period and in 100 non-hyperbilirubinemic G-6-PD deficient newborn infants, at the age of 12 months or more. Six subjects in the first group and 13 in the second were found to be carriers of the beta-thalassemia trait. Statistical analysis of the data did not show any significant difference between the two groups. It seems that the beta-thalassemia trait does not provide any protection against neonatal hyperbilirubinemia associated with G-6-PD deficiency.

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“…In all the cases studied, no sign of marked hemolysis, independent of the bilirubin level, was observed. The same finding also characterized a group of jaundiced newborns, with the same erythrocyte enzyme deficiency, on whom light therapy was per formed [10]. In the above mentioned surveys, the red cell turnover was estimated by controlling the hemoglobin (Hb) and/or hematocrit (Ht) val ues.…”

mentioning

confidence: 76%

Haptoglobin, Hemopexin, Hemoglobin and Hematocrit in Newborns with Erythrocyte Glucose-6-Phosphate Dehydrogenase Deficiency

Meloni¹,

Costa²,

Cutillo³

1975

Acta Haematol

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Hemolysís was studied in 40 G-6-PD-deficient newborn infants, half of whom had bilirubin blood levels within the normal range whereas the others, who were hyperbilirubinemic, underwent exchange transfusion. Hemoglobin, hematocrit, hemopexin and haptoglobin showed no or little differences between either of the two groups and the controls. The findings confirm the authors’ assumption expressed elsewhere that this form of hyperbilirubinemia is not hemolytic in nature.

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Phototherapy for neonatal hyperbilirubinemia in mature newborn infants with erythrocyte G-6-PD deficiency

Cited by 14 publications

References 4 publications

Rhesus disease: postnatal management and outcome

Rhesus disease: postnatal management and outcome

β-Thalassemia trait and hyperbilirubinemia in G-6-PD deficient newborn infants

Haptoglobin, Hemopexin, Hemoglobin and Hematocrit in Newborns with Erythrocyte Glucose-6-Phosphate Dehydrogenase Deficiency

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