The Le(a) antigen and neonatal hyperbilirubinemia in Taiwan

Vox Sanguinis
M LinD C Liang

Abstract

Neonatal jaundice is known to be more severe in Taiwanese infants than in Caucasian infants. Although ABO fetomaternal incompatibility and glucose-6-phosphate dehydrogenase deficiency have been shown to play a role in the etiology of neonatal jaundice in some Taiwanese infants, the etiology in the majority of cases is unknown. In this study we found that in Taiwanese newborn infants, the red cell Le(a) antigen appeared later in infants who were jaundiced (peak serum bilirubin levels of > 12 mg/dl during the first week of life) than in infants who were not. However, the Leb antigen, and hence the transferase encoded by the Se and Se(w) genes, did not appear to be similarly involved in the etiology of physiological jaundice. Thus it would appear that the Le gene-specified transferase is less active or has a delayed function, in jaundiced infants. The relationship between the Le gene-specified transferase and bilirubin has yet to be established.

References

Jan 1, 1991·Human Heredity·R E Broadberry, M Lin-Chu
Jan 1, 1988·Human Heredity·S M HenryD G Woodfield
Dec 1, 1993·Immunology and Cell Biology·W G AbbottA Geursen

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Citations

Aug 6, 2008·The Journal of the Royal Society for the Promotion of Health·David B ShortlandAshoka Dey Chowdhury
Feb 14, 1998·Transfusion Medicine Reviews·M Lin, R E Broadberry

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