IN NEWBORN INFANTS
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CSF was obtained from a total of 52 newborn infants by lumbar puncture for diagnostic reasons or post mortem. At the same time a venous blood sample was taken. The infants were divided into two groups: i) "bilirubinemia", including all cases of hyperbilirubi nemia and infants presumably without CNS affection (prematurity, RDS, malformations); ii) "CNS affection", including all cases of intracranial hemorrhages and infants suffering from meningitis, sepsis, and congenital toxoplasmosis. Tot~l BR in serum and CSF was determined by standard laboratory methods, CSF-BR was additional ly assayed according to van Roy et al.2, with separation of diazo tized dipyrroles by thin layer chromatogra?hy. Estimation of BR unbound to albumin (free BR) was performed by the peroxidase tech nique3, albumin was estimated by bromocresol green binding4 .
[1] R. Wennberg,et al. Determination of unbound bilirubin in the serum of newborns. , 1974, Clinical chemistry.
[2] K. Kjellin. The binding of xanthochromic compounds in the cerebrospinal fluid. Preliminary report. , 1969, Journal of the neurological sciences.
[3] F. de Meuter,et al. Determination of bilirubin in liver homogenates and serum with diazotized p-iodoaniline. , 1971, Clinica chimica acta; international journal of clinical chemistry.
[4] J. Lucey. Bilirubin and Brain Damage— A Real Mess , 1982, Pediatrics.