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Glucose‐6‐Phosphate Dehydrogenase Deficiency and Neonatal Jaundice in Jamaica
Author(s) -
Gibbs W. N.,
Gray R.,
Lowry M.
Publication year - 1979
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1979.tb03750.x
Subject(s) - jaundice , kernicterus , glucose 6 phosphate dehydrogenase deficiency , medicine , abo incompatibility , pediatrics , exchange transfusion , abo blood group system , incidence (geometry) , glucose 6 phosphate dehydrogenase , hypoglycemia , glucosephosphate dehydrogenase deficiency , disease , gastroenterology , dehydrogenase , enzyme , biology , biochemistry , insulin , physics , optics
S ummary . Glucose‐6‐phosphate dehydrogenase (G6PD) deficiency was detected in 16 (69.6%) of a group of 23 neonates who had unexplained moderate or severe jaundice. This proportion is significantly more than the 9.4% observed or the 22.2% expected in Jamaican neonates who are not moderately or severely jaundiced ( P <0.003), and significantly more than the 12.6% observed or the 21.0% expected in older Jamaican children and adults ( P <0.003). Phenobarbitone therapy and phototherapy reduced the need for exchange transfusion but this was necessary in eight patients. Two babies developed kernicterus and one died. On the other hand, only two of 21 neonates who were identified as G6PD deficient at birth subsequently became moderately or severely jaundiced, and this could be attributed to other causes in both cases. These findings indicate that apparently spontaneous neonatal juandice is important in infants who have the G6PD A— enzyme. However, the jaundice is probably precipitated by unknown factors to which the G6PD deficient neonate is more susceptible than the infant who is not G6PD deficient. There is also a slightly increased incidence of G6PD deficiency in neonates who develop jaundice because of ABO or Rh(D) iso‐immune disease, infection or prematurity.