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Breast milk β‐glucuronidase and prolonged jaundice in the neonate
Author(s) -
Ince Z,
Coban A,
Peker I,
Can G
Publication year - 1995
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1995.tb13621.x
Subject(s) - medicine , jaundice , breast milk , breast feeding , gastroenterology , glucuronidase , physiology , endocrinology , enzyme , pediatrics , biochemistry , biology
Breast milk samples from mothers of breast‐fed, healthy, term newborns with unexplained prolonged jaundice were analyzed for β‐glucuronidase activity. Mean enzyme activity was 75.7 ± 34.5 modified Sigma units/ml in the breast milk samples ingested by the study group of jaundiced babies ( n = 25) and 82.2 ± 40.1 modified Sigma units/ml in the samples ingested by the control group of non‐jaundiced babies ( n = 20) ( p > 0.05). Enzyme activities at 2, 3 and 4 postnatal weeks were 101.0 ±39.9, 66.0 ± 20.7 and 57.0 ± 22.4 modified Sigma units/ml in the study group and 87.9 ±36.1, 58.5 ± 15.0 and 88.3 ±49.1 modified Sigma units/ml in the controls. The differences were not statistically significant ( p > 0.05). We conclude that breast milk β‐glucuronidase activity may be a contributory factor, in the presence of other variables, in hyperbilirubinemia but it is neither the main nor the only cause of prolonged jaundice in neonates.