Jaundice neonatal

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... 

Necheles et al. (N4) first reported a genetically determined homozygous GSH-Px deficiency associated with neonatal jaundice and mild hemolysis. Spontaneous recovery from hemolysis was noted 3 months after birth. Thereafter, several cases with GSH-Px deficiency were reported. Newborn infants exhibit significantly lower red blood cell GSH-Px activity and serum selenium concentrations than adult control subjects, and a significantly positive correlation between selenium concentration and GSH-Px activity has been observed. Furthermore, the addition of selenium stimulates, both in vivo and in vitro, the GSH-Px activity. The neonatal red blood cell GSH-Px deficiency may be partially due to insufficient availability of selenium during pregnancy (P9). Therefore, the diagnosis of GSH-Px deficiency in newborn infants must be made carefully. 

Damm D, Grandjean P, Lyngbye T, et al. 1993. Early lead exposure and neonatal jaundice relation to neurobehavioral performance at 15 years of age. Neurotoxicol Teratol 15 173-181. 

Several other metal complexes have promising photodynamic activity and are currently under development (248). Metalloporphyrins inhibit the enzyme heme oxygenase for example, chromium porphyrin and mesoporphyrin are potent inhibitors of heme oxygenase both in vitro and in vivo (249, 250) and are being used for the treatment of the neonatal jaundice. 

Outline the importance the photochemistry of C=C bonds in the phototherapy of infants with neonatal jaundice, the process of vision and the effects of ultraviolet radiation on DNA. 

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. 

Doan HM, Keith L, Shennan AT. 1979. Phenol and neonatal jaundice. Pediatrics 64 324-325. 

Rl. Ramboer, C., Thompson, R. P. H., and Williams, R., Controlled trials of pheno-barbitone therapy in neonatal jaundice. Lancet i, 966-968 (1969). 

Kallen and Robert (2000) found no adverse effects on congenital malformations, childhood cancer, infant mortality, low Apgar score, neonatal jaundice, or neonatal hypothyroidism among infants and children who lived in areas where drinking water was disinfected with chlorine dioxide, compared to controls living in... 

Phototherapy is the generic term covering therapies which use light either with or without a sensitiser. Those that do not require a sensitiser use the natural chromophores within the tissue to perform this function e.g. treatment of vitamin D deficiency in rickets, and neonatal jaundice). Those that do use an added sensitiser include photochemotherapy (largely psoriasis and skin disorders) and photodynamic therapy (currently mainly cancer). Photodynamic therapy is differentiated from photochemotherapy by its additional requirement for the presence of oxygen at molecular or ambient levels.In this text we will deal only with photodynamic therapy since, at the present time, this is the main driving force in phototherapy. ° ... 

Lower-than-normal activities are often obtained in newborns and in preterm and small-for-age infants [12, 23], especially if they have neonatal jaundice [22]. Plasma biotinidase activity increases with advancing age, reaching maximum values at between 20 and 40 days [23]. 

Schulpis KH, Gavrili S, Tjamouranis J, Karikas GA, Kapiki A, Costalos C ( 2003) The effect of neonatal jaundice on biotinidase activity. Early Hum Dev 72 15-24... 

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. 

Alterations in the metabolism of heme. A. Hemolytic jaundice. B. Neonatal jaundice. [Note The enterohepatic circulation of urobilinogen is omitted for simplicity.] BG = bilirubin glucuronide B = bilirubin U = urobilinogen S = stercobilin. 

Hemolytic jaundice Obstructive jaundice Hepatocellar jaundice Neonatal jaundice... 

Definition and causes of jaundice Jaundice (icterus) refers to the yellow color of the skin, nail beds, and sclerae caused by deposition of bilirubin, secondary to increased bilirubin levels in the blood. There are three major forms of jaundice hemolytic jaundice, caused by massive lysis of red blood cells, releasing more heme than can be handled by the reticuloendothelial system obstructive jaundice, resulting from obstruction of the bile duct and hepatocellular jaundice, caused by damage to liver cells that decreases the liver s ability to take up and conjugate bilirubin. In addition, neonatal jaundice is caused by the low activity of hepatic glucuronylation of bilirubin, especially in premature infants. 

Isomerism can also be induced phulochemically, although such processes are less well understood and probably require the presence of additional free radicals. The cytotoxic metabolite bilirubin can cause brain damage in infants with neonatal jaundice this is prevented by exposing the child to intense blue light. The bilirubin is photochemically converted in the skin to metastable geometric isomers, which can be transported in the blood and excreted in bile. 

The incidence of neonatal jaundice was not increased after induction of labor with prostaglandins (47). 

Lange AP, Secher NJ, Westergaard JG, Skovgard I. Neonatal jaundice after labour induced or stimulated by prostaglandin E2 or oxytocin. Lancet 1982 l(8279) 991-4. 

L3. Lathe, G. H., and Walker, M., An enzyme defect in human neonatal jaundice and in Gunn s strain of jaundiced rats. Biochem. J. 66, 9 P (1957). 

In an earlier study by Wolfe et al. (1985) of Air Force personnel involved in Operation Ranch Hand, a significant increase in the number of reported neonatal deaths (no additional details provided), as compared to a comparison group of Air Force military employees not stationed in Vietnam, was observed. The incidence of major defects, prematurity, learning disabilities, or infant deaths was not increased in the Ranch Hand personnel. A significant increase in the incidence of minor health effects such as birth marks, rashes, and neonatal jaundice was reported by the Ranch Hand veterans. It should be noted that the pregnancy outcomes were self-reported, and this finding was not corroborated by the follow-up study (Wolfe et al. 1995) which used birth certificates, medical records, and death certificates to assess possible relationships between paternal exposure to 2,3,7,8-TCDD and developmental effects in offspring. 

Storm, W. 1990. Human milk feeding and neonatal jaundice. Kinderkrankenschwester 9, 52-53. 

A condition similar to the Crigler-Najjar syndrome, though of only a temporary nature, is neonatal jaundice, which exists when the newborn (especially a... 

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