title: [Neonatal hyperbilirubinemia and molecular mechanisms of jaundice].
abstract: 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.
authors.affiliation: Centrum experimentální medicíny IKEM Praha. milan.jirsa@ikem.cz
authors.forename: M
authors.initials: M
authors.lastname: Jirsa
authors.forename: E
authors.initials: E
authors.lastname: Sticová
mesh_terms: D001663:Bilirubin / Q000378:metabolism*; D003414:Crigler-Najjar Syndrome / Q000378:metabolism*; D006801:Humans; D006933:Hyperbilirubinemia, Hereditary / Q000378:metabolism*; D051556:Hyperbilirubinemia, Neonatal / Q000145:classification / Q000378:metabolism*; D007231:Infant, Newborn; D007565:Jaundice / Q000145:classification / Q000378:metabolism; D007566:Jaundice, Chronic Idiopathic / Q000145:classification / Q000378:metabolism*; D007567:Jaundice, Neonatal / Q000145:classification / Q000378:metabolism*
chemical_list: D001663:Bilirubin