Insufficient Glucuronide Formation in the Newborn and its Relationship to the Pathogenesis of Icterus Neonatorum

Hyperbilirubinemia and urinary D-glucaric acid excretion in premature infants following antepartum dexamethasone treatment

“…The present study was, therefore, undertaken to evaluate the effect of maternally administered dexamethasone on the serum bilirubin levels of premature infants. Since the hepatic microsomal enzyme glucuronyl transferase (UDPGT), which is immature in the newborn infant [1, 8,24], plays a key role in the metabolism of both bilirubin and glucocorticoids [7], it was also of some interest to provide additional data by studying the influence of prenatal dexamethasone treatment on the urinary D-glucaric acid excretion of infants bom prematurely.…”

Bilirubin Clearance in Healthy and Pathological Newborns

“…On the first day, an average of 35% of the administered bili rubin was retained in the circulation in 3-h specimens, whereas on the 5th day of life, bilirubinemia dropped within I h to the initial level and sometimes even below it. Thus, the ability to remove unconjugated bilirubin from the serum increases within the first week of life, which corresponds with the in creasing capacity of the liver to form glucuronides [Vest, 1958]. In older children (8 months to 15 years) [W eech and Van d .…”

Endogenous production of carbon monoxide in normal and erythroblastotic newborn infants

“…Jaundice in the normal newborn infant has been attributed to the inability of the liver to conjugate bilirubin due to decreased activity of the glucuronyltransferase enzyme (46)(47)(48) in the face of a relatively "normal" rate of bilirubin production. However, our results indicate that normal newborns produce bilirubin at more than twice the adult rate (per kilogram per 24 hr).…”