[Neonatal hyperbilirubinemia and molecular mechanisms of jaundice].

Vrozené hyperbilirubinemie a molekulární mechanizmy žloutenky.

Publisher: Ambit Media Country of Publication: Czech Republic NLM ID: 0413602 Publication Model: Print Cited Medium: Print ISSN: 0042-773X (Print) Linking ISSN: 0042773X NLM ISO Abbreviation: Vnitr Lek Subsets: MEDLINE

Publication: 2010- : Brno : Ambit Media
Original Publication: 1973-<1994> : Praha : Avicenum

Bilirubin/*metabolism ; Crigler-Najjar Syndrome/*metabolism ; Hyperbilirubinemia, Hereditary/*metabolism ; Hyperbilirubinemia, Neonatal/*metabolism ; Jaundice, Chronic Idiopathic/*metabolism ; Jaundice, Neonatal/*metabolism; Humans ; Hyperbilirubinemia, Neonatal/classification ; Infant, Newborn ; Jaundice/classification ; Jaundice/metabolism ; Jaundice, Chronic Idiopathic/classification ; Jaundice, Neonatal/classification

The introductory summarises the classical path of heme degradation and classification of jaundice. Subsequently, a description of neonatal types of jaundice is given, known as Crigler Najjar, Gilberts, DubinJohnson and Rotor syndromes, emphasising the explanation of the molecular mechanisms of these metabolic disorders. Special attention is given to a recently discovered molecular mechanism of the Rotor syndrome. The mechanism is based on the inability of the liver to retrospectively uptake the conjugated bilirubin fraction primarily excreted into the blood, not bile. A reduced ability of the liver to uptake the conjugated bilirubin contributes to the development of hyperbilirubinemia in common disorders of the liver and bile ducts and to the toxicity of xenobiotics and drugs using transport proteins for conjugated bilirubin.

RFM9X3LJ49 (Bilirubin)

Date Created: 20130806 Date Completed: 20151030 Latest Revision: 20181202

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