Bilirubin neonatal

Bilirubin oxidase [80619-01 -8], derived from Mjrothecium verrucaria, was modified with polyethyleneglycol when this conjugate was injected intravenously to jaundiced rats, the plasma bilirubin dropped to normal levels. This approach might have potential in the treatment of hyperbilimbinemia, fulminant hepatitis, and neonatal bilirubin encephalopathy (177). 

Kaplan M, Hammerman C, Maisels MJ Bilirubin genetics for the nongeneticist hereditary defects of neonatal bilirubin conjugation. Pediatrics 111 886-893,2003. 

Neonatal-bilirubin E98, E104, El 16, E562, E569, EN48, EN109. 

E86 Ou, C.-N., Gilman, G.E. and Buffone, G.J. (1982). Evaluation of a neonatal bilirubin assay on the Kodak Ektachem analyzer. Clin. Chem. 28, ISS3, Abstr. 20. 

E2I9 Mueller, K.W. (1985). Neonatal bilirubin correlation Ektachem NBIL vs. ACA III TBIL. Clin. Chem. 31,988, Abstr. 445. 

EN48 Langbaum, M., Farber, S. and Rosenthal, P. (1991). Kodak Ektachem total bilirubin and neonatal bilirubin measurements in newborns - is a distinction clinically relevant Clin. Chem. 37, 987-988, Abstr. 370. 

Harding, R., Virapen, K. and O Brien, P. (1982). Evaluation of neonatal bilirubin assays on the Ames Seralyzer. Clin. Biochem. 15, 100, Abstr. 61. 

Yeung, C., Lee, F., and Wong, H. 1990. Effects of a popular Chinese herb on neonatal bilirubin protein bindin. Biol. Neonate 58, 98-103. 

Neonatal bilirubin levels and glucose-6-phosphate dehydrogenase deficiency in preterm and low-birth-weight infants in Israel. 

Neonatal bilirubin production-conjugation imbalance effect of glucose-6-phosphate dehydrogenase deficiency and borderline prematurity. 

Mielsch, C., Zimmermann, A., Wagner, D., Matthes, B., Schlebusch, H., Luppa, P.B., 2010. Point-of-care determination of neonatal bilirubin with tbe blood gas analyzer RapidLab 1265. Clin. Cbem. Lab. Med. 48, 1455-1461. bttp //dx.doi.org/10.1515/ CCLM.2010.279. 

Hyjjerbilirubinaemia is an abnormality observed mainly in neonates in whom the liver is insufficiently developed to be able to detoxify the bile pigment bilirubin. This situation is known as neonatal jaundice and can sometimes become a serious disease causing neurotoxic symptoms. Bilirubin is produced by the degradation of heme [the Fe(II) complex of protoporphyrin IX] by heme oxygenase to give biliverdin, which is reduced by biliverdin reductase to... 

Host factors can help to ensure selection of the most appropriate antimicrobial agent. Age is an important factor in antimicrobial selection. With regard to dose and interval, renal and hepatic function varies with age. Populations with diminished renal function include neonates and the elderly. Hepatic function in the neonate is not fully developed, and drugs that are metabolized or eliminated by this route may produce adverse effects. For example, sulfonamides and ceftriaxone may compete with bilirubin for binding sites and may result in hyperbilirubinemia and kernicterus. Gastric acidity also depends on... 

Akaba K, Kimura T, Sasaki A et al. Neonatal hyperbilirubinemia and mutation of the bilirubin uridine diphosphate-glu-curonosyltransferase gene a common missense mutation among Japanese, Koreans and Chinese. Biochem Mol Biol Int 1998 46 21-26. 

Bilirubin is a product of the breakdown of haemoglobin in red blood cells. Neonatal jaundice occurs when bilirubin builds up faster than a newborn baby s liver is able to break it down. This results in the deposition of water-insoluble bilirubin in the skin (giving the skin a yellow colour) and untreated it can lead to damage of the central nervous system by deposition in brain cells. 

The over-production of bilirubin to the point at which the liver s capacity to metabolize is exceeded or if there is dysfunction of the liver itself due to damage or metabolic immaturity, can lead to a yellow discolouration of tissues called jaundice. The accumulation of unconjugated bilirubin in neonates, often as a result of antibody-mediated destruction of the baby s red cells is dangerous as serious and irreversible brain damage can occur. Acute or chronic damage to the adult liver (hepatitis) may cause jaundice but not brain damage. 

Conjugation with glucuronyl residues is of great importance for the metabolic fate of bilirubin (S3), steroids (L5, M2, R8), catecholamines (W17) and other hydrophobic compounds (D8, D9). Neonatal accumulation of bilirubin in man and rats may trigger maturation of UDP-glucuronyltransferase (Bl, B2, T6). Delayed maturation of the enzyme, or its partial or total deficiency, are critical factors in the development of kernicterus (P6). Compared to other species partial deficiency of the... 

There is considerable variation in the protein binding among the cephalosporins. Drugs like ceftriaxone that have extensive protein binding (85-95%) may displace bilirubin from serum albumin. Consequently, ceftriaxone may increase the risk of kemicterus in jaundiced neonates. 

Neonatal jaundice Babies with G6PD deficiency may experience neonatal jaundice appearing one to four days after birth. The jaundice, which may be severe, results from impaired hepatic catabolism of heme or increased production of bilirubin. 

---