Sequelae of neonatal jaundice.

Abstract

Two parameters of connective tissue metabolism, viz. urinary hydroxyproline and urinary glycosaminoglycans, have been studied in newborn babies. A characteristic pattern is discernible, which is probably related to the rate of growth. The precise clinical value of these observations is yet to be determined, but it seems probable that they will provide a useful assessment of 'chemical growth' in the newborn.

Factors affecting neonatal jaundice.

“…17 of 18 children found to be deaf by Fenwick (1975) after similar PB levels had haemolytic disease and, in the 18th, the child's mother had an obscure jaundice. In an earlier series of 371 jaundiced infants reported by us (Culley et al, 1970), full neurological and psychomotor examination at age 5 years showed no ill effects unless PB exceeded 342 ,umol/l (20 mg/100 ml).…”

Neonatal non-hemolytic hyperbilirubinemia: a prevalence study of adult neuropsychiatric disability and cognitive function in 463 male Danish conscripts

“…Some of the studies were conducted within fractions of the Perinatal Collaborative Project comprising 56 990 pregnant women 1–7. The findings have not been uniform, but most often no association was found.…”

“…The findings have not been uniform, but most often no association was found. A possible reason for divergent observations may be inclusion by many studies of preterm infants and/or infants with Rhesus isoimmunisation 1–7. Four studies have restricted the analyses to full-term newborns with non-hemolytic hyperbilirubinemia 8 11–13.…”

“…The generalisability of many studies has been limited by the inclusion of preterm infants and/or infants with hemolytic hyperbilirubinemia,1–7 9 or by a small number of subjects 8 9. Only two studies had a follow-up of more than 13 years 9 10…”

Sequential Trial of Effect of Phenobarbitone on Serum Bilirubin of Preterm Infants

“…Children who develop severe hyperbilirubinaemia are liable to have later evidence of brain damage (Boggs, Hardy, and Frazier, 1967;Hyman et al, 1969;Culley et al, 1970). This brain damage becomes more likely when the peak serum bilirubin level rises above 16 mg/100 ml.…”