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Neonatal Hyperbilirubinemia

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... [Pg.1028]

Phototherapy The use of ultraviolet light applied to the skin, for example in treating psoriasis or neonatal hyperbilirubinemia. [Pg.1574]

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. [Pg.307]

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... [Pg.946]

Daum F, Cohen MI, McNamara H, et al. 1976. Experimental toxicologic studies on a phenol detergent associated with neonatal hyperbilirubinemia. J Pediatr 89 853-854. [Pg.207]

Wysowski DK, Flynt JW, Goldfield M, et al. 1978. Epidemic neonatal hyperbilirubinemia and use of a phenolic disinfectant detergent. Pediatrics 61 165-170. [Pg.231]

AlO. Arias, I. M., Gartner, L. M., Seifter, S., and Furman, M., Prolonged neonatal unconjugated hyperbilirubinemia associated with breast feeding and a steroid, pregnane-3a,20/3-diol, in maternal milk that inhibits glucuronide formation in vitro. J. Clin. Invest. 43, 2037-2047 (1964). [Pg.278]

Liver disease is commonly associated with oq-antitrypsin deficiency and may develop at any age. Approximately 10% to 20% of oq-antitrypsin-deficient infants with the phenotype PIZZ are first seen for neonatal cholestatic liver disease, as was the child in this case report. Conjugated hyperbilirubinemia and he-... [Pg.44]

As in case 2, some patients with G6PD variants experience hyperbilirubinemia in the neonatal period. Neonates with the rare class I variant are particularly at risk, but more common variants account for the majority of cases. The... [Pg.130]

Hyperbilirubinemia in newborn infants is very common and accounts for most of the laboratory testing done in the neonatal period. The greatest challenge to managing neonates with hyperbilirubinemia is the short hospital stay of mothers and infants. The length of stay is as little as 24 h in some cases, which does not allow adequate time for the normal bilirubin rise to occur. This requires the physician to make a diagnosis quickly and accurately but sometimes with only limited laboratory data. [Pg.234]

The gestational age of the infant is a major factor in the development of neonatal hyperbilirubinemia. The more premature the infant is, the lower the level of expression of the enzymes necessary for synthesis of conjugated bilirubin (discussed in the section on Hepatic Metabolism of Bilirubin) and the more likely the child is to develop jaundice. Babies are not routinely screened for the cause of jaundice until the condition manifests itself. Testing would be instituted early if there were a sibling who had experienced prolonged jaundice, or if the mother is blood type O or is Rh negative. All mothers who have good prenatal care are tested for blood type and Rh antibodies. This alerts the physician to potential problems and allows the physician to anticipate the most common forms of jaundice, namely, ABO incompatibilities. [Pg.235]

One needs to keep in mind that the use of drugs by the mother will sometimes lead to impairment of the activity of bilirubin-UDP-glucuronyltransferase. Phenothiazines are an example of this kind of interaction. The use of drugs in the neonatal intensive care unit also can contribute to hyperbilirubinemia. Usually, the medications that compete for binding sites on albumin are the culprits in this case (see section on Bilburin Transport). An example of this type of interaction is the use of furosimide, which is a diuretic used to decrease fluid retention and improve cardiac function and renal output. [Pg.236]

For many years, phototherapy has been the standard treatment of neonatal hyperbilirubinemia. The effectiveness of this form of therapy is based on the ability of photons of the appropriate wavelength to convert the intramolecularly H-bonded bilirubin IXa with its low solubility into photoisomers of bilirubin in which the normal Z,Z stereochemistry at the 4- and 15-positions is changed, resulting in photoisomers that are more water soluble. In addition, bilirubin can be converted into the cyclic lumirubin, which is soluble and can be excreted in the urine (Fig. 22-2). Photoproducts can also be excreted through the liver pathway without... [Pg.240]

Dennery PA, Seidman DS, Stevenson DK Neonatal hyperbilirubinemia.NEnglJMed 344 581-590, 2001. [Pg.242]

Ip S, Chung M, Kulig J, et al. An evidence-based review of important issues concerning neonatal hyperbilirubinemia. Pediatrics 114 130-153, 2004. [Pg.242]

Dehydrogenase Deficiency, Biotinidase Deficiency, and Adrenoleukodystrophy. Catabolism of essential amino acid skeletons is discussed in the chapters Phenylketonuria and HMG-CoA Lyase Deficiency. The chapters Inborn Errors of Urea Synthesis and Neonatal Hyperbilirubinemia discuss the detoxification and excretion of amino acid nitrogen and of heme. The chapter Gaucher Disease provides an illustration of the range of catabolic problems that result in lysosomal storage diseases. Several additional chapters deal with key aspects of intracellular transport of enzymes and metabolic intermediates the targeting of enzymes to lysosomes (I-Cell Disease), receptor-mediated endocytosis (Low-Density Lipoprotein Receptors and Familial Hypercholesterolemia) and the role of ABC transporters in export of cholesterol from the cell (Tangier disease). [Pg.382]

These include postnatal depression and acute dystonic reactions (which may interfere with normal delivery). Hypotonia can persist for months (569) and may respond to diphenhydramine 5 mg/kg/day. Severe rhinorrhea and respiratory distress in a neonate exposed to fluphenazine hydrochloride prenatally has been reported (484). Neonatal jaundice, hyperbilirubinemia, and melanin deposits in the eyes have occurred when neuroleptic drugs were given during the last trimester or longer during pregnancy. [Pg.229]


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See also in sourсe #XX -- [ Pg.130 ]




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