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Gilbert's Syndrome (gilbert + syndrome)
Selected AbstractsPresence of the genetic marker for Gilbert syndrome is associated with increased level and duration of neonatal jaundiceACTA PAEDIATRICA, Issue 1 2002N Roy-Chowdhury No abstract is available for this article. [source] Study of in vitro glucuronidation of hydroxyquinolines with bovine liver microsomesFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2002Masanobu Kanou Abstract Glucuronidation of drugs by UDP-glucuronosyltransferase (UGT) is a major phase II conjugation reaction. Defects in UGT are associated with Crigler,Najjar syndrome and Gilbert's syndrome with severe hyperbilirubinaemias and jaundice. We analysed the reactivities of some hydroxyquinoline derivatives, which are naturally produced from quinoline by cytochrome P450. The analyses were carried out using a microassay system for UGT activity in bovine liver microsomes in the range 0.5,100 pmol/assay with the highly sensitive radio-image analyser Fuji BAS2500 (Fujifilm, Tokyo, Japan). 3-Hydroxylquinoline is a good substrate for glucuronidation, and the relative Kcat values were 3.1-fold higher than the values for p-nitrophenol. 5,6-Dihydroquinoline-5,6- trans -diol gave a similar Km value to that of 3-hydroxyquinoline, but the Vmax value was approximately 1/15 of that of p-nitrophenol and showed weak reactivity. Quinoline N-oxide gave a low Vmax value and showed marginal activity. The Kcat values of 6-hydroxyquinoline and 5-hydroxyquinoline were 2.1- and 1.2-fold higher than that of p-nitrophenol, respectively. Fluoroquinoline (FQ) derivatives, such as 3FQ, 7,8diFQ and 6,7,8triFQ, did not show any substrate activities. These results suggest that there are therapeutic problems in administration of some quinoline drugs to patients with jaundice. [source] What is Gilbert's syndrome?JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2004Lesson from genetic polymorphisms of UGT1A1 in Gilbert's syndrome from Asia [source] Role of UGT1A1 mutation in fasting hyperbilirubinemiaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2001Tomoaki Ishihara Abstract Background and Aim: Low-grade fasting hyperbilirubinemia is a common observation in healthy subjects (HS), whereas high-grade fasting hyperbilirubinemia is believed to be a characteristic finding of Gilbert's syndrome. This study was undertaken to assess the role of mutation in bilirubin UDP- glycosyltransferase gene (UGT1A1) on fasting hyperbilirubinemia. Methods: Analysis of UGT1A1 and a caloric restriction test (400 kcal for 24 h) were performed in 56 healthy subjects (25 males, 31 females), and 28 patients with Gilbert's syndrome (18 males, 10 females). There were 29 healthy subjects with no mutation in UGT1A1, and 27 healthy subjects and 26 Gilbert's syndrome patients with mutations in the coding and/or promoter (TATA box) regions of UGT1A1. Results: The mean increment of serum bilirubin (,SB) was 9.6 ,mol/L (males) and 4.1 ,mol/L (females) in subjects with no UGT1A1 mutation. Subjects with mutation in UGT1A1 showed higher levels of ,SB than individuals without mutation. Among healthy subjects, gender difference in ,SB values was observed only in individuals with the wild type of UGT1A1, but not in those with mutations in this gene. Conclusion: The results of the present study suggest that UGT1A1 mutation has a role in the development of high-grade fasting hyperbilirubinemia after caloric restriction. [source] | ||||||||||