Jaundice, newborn

New impetus was given to photomedicine by development of lasers that are compatible with the clinical environment. These include HeNe, Ar ion, mby, and tunable dye lasers operating in the continuous wave (cw) mode. Prior to the advent of lasers in medicine, only the treatment of newborn jaundice, and the appHcation of long wavelength uv irradiation in conjunction with adininistration (or topical appHcation) of psoralen class sensitizers to treatment of skin diseases (86), principally psoriasis, were clinically important phototherapies. 

Newborn jaundice, photochemical treatment of, 79 120 New chemicals, pricing of, 75 641-642 New Chemicals Program (EPA), 9 456 New Drug Application (NDA), 27 574 New drug approval (NDA) process, 78 698-701... 

Jaundice is notitseifa disease but is an important diagnostic indicator of many underiying conditions, in newborns, jaundice can iead to toxic encephalopathy due to deposition of bilirubin within the lipid regions of membranes of the brain (kernicterus). 

After approx. 10 days, newborn jaundice subsides without any further consequences. Bilirubin also acts as an antioxidant and can thus provide protection from oxygen radicals, if necessary. Peripartal complications can, however, reinforce or prolong this state. This may occur in infantile hypothyroidism or when medication is administered directly to the infant as well as via breast milk (particularly when bilirubin is displaced from its albumin binding by drugs). In more pronounced jaundice, phototherapy and an increase in the oral intake of fluids may be advisable. (44, 45, 48,53,58, 64)... 

Jaundice of newborn Jaundice of prematurity Gilbert syndrome Crigler-Najjar syndrome... 

Encyclopedia Newborn jaundice httpvywww.nlm.nih.gOv/medlineplus/ency/aiticle/001559.htm... 

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. 

The forms of phototherapy in common use include (i) the phototherapy of jaundice (neonatal hyperbilirubinemia) in the newborn, and especially in the prematurely born 5 (ii) the treatment of psoriasis using light in the UV-A range (320 100 nm) and an administered photosensitizer, such as 8-methoxypsoralen 6 (iii) the treatment of the wet form of age-related macular degeneration with a photosensitizer such as a benzoporphyrin derivative (VISUDYNE ), and a laser light source 7 and (iv) the treatment of certain cancers with a photosensitizer such as a porphyrin derivative, and red light.8... 

Other Disorders Discussed in Relation to Hereditary G-6-PDH Deficiency, Severe hemolytic jaundice in newborns without incompatibility either in classic blood groups or in the rhesus Systran, but... 

The activity of glucuronidation is low in the newborn, especially in premature babies (6). This is evident in the jaundice observed in many newborns because the major clearance pathway for bilirubin is glucuronidation. This can also lead to increased toxicity of some drugs in the newborn such as the grey baby syndrome seen in newborns treated with chloramphenicol. 

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. 

A second series of reports in the literature purport to discuss the toxicity of phenol to newborns. These, however, deal with an excessive level of hyperbilirubinemia, or jaundice, in newborns in hospital nurseries where a phenolic disinfectant detergent was used to clean the nursery and its equipment (bassinets and mattresses) (Doan et al. 1979, Wysowski et al. 1978). Review of these reports indicated that the detergent did not contain phenol per se. rather it contained more complex phenolics such as o-benzyl-p-chlorophenol and p-tertiary amylphenol. 

Physiologic jaundice in the newborn, especially premature infimts (enzymes may not be fuUy induced)... 

Parenteral Anticoagulant-induced prothrombin deficiency hypoprothrombinemia secondary to conditions limiting absorption or synthesis of vitamin K (eg, obstructive jaundice, biliary fistula, sprue, ulcerative colitis, celiac disease, intestinal resection, cystic fibrosis of the pancreas, regional enteritis) drug-induced hypoprothrombinemias due to interference with vitamin K metabolism (eg, antibiotics, salicylates) prophylaxis and therapy of hemorrhagic disease of the newborn. 

Children Safety and efficacy in children have not been established. Hemolysis, jaundice, and hyperbilirubinemia in newborns, particularly in premature infants, have been reported with vitamin K. These effects may be dose-related. Therefore, do not exceed recommended dose. 

Toxicity of vitamin K has not been well defined. Jaundice may occur in a newborn if large dosages of vitamin K are given to the mother before birth. Although kemicterus may result, this can be prevented by using vitamin K. 

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]. 

It is generally accepted that in normal subjects, most, but not necessarily all, of the bilirubin formed results from the breakdown of hemoglobin in the reticuloendothelial system. The bilirubin is then conjugated in the liver and excreted into the bile as a water-soluble pigment. The capacity of the liver to conjugate bilirubin is limited (W6), so that in cases of overproduction (e.g., hemolytic jaundice) free bilirubin will appear in the plasma. A similar result will be obtained if the ability of the liver to conjugate bilirubin is diminished (e.g., in the newborn infant). On the other hand, if the excretion of the bile is for some reason... 

The use of the icterus index, as described by Meulengracht, for the assessment of jaundice has fallen into disrepute because of the errors caused by the presence of lipochromes, carotenoids, and other yellow pigments. Josephson (J6) in his survey found that the correlation coefficient between icterus index and serum bilirubin concentration was 0.69 in 360 healthy subjects and 0.84 in 40 jaundiced subjects. In newborn infants however, bilirubin is the only yellow pigment likely to be present and the possibility of determining serum bilirubin concentrations by direct measurement has again been re-examined. Abelson and Boggs (Al) diluted serum from infants with erythroblastosis 1 in 50 and studied the absorption curves. They found that in addition to the bili-... 

Stempfel, R., Broman, B., Escardo, F., and Zetterstrom, R., Obstructive jaundice complicating hemolytic disease of the newborn. Pediatrics 17, 471-481 (1956). 

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

A newborn child was found to be lethargic and jaundiced and, at 6 days of age, showed elevated blood phenylalanine levels. He was placed on a low-phenyla-... 

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