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Contribution of the TATA-Box Genotype (Gilbert Syndrome) to Serum Bilirubin Concentrations in the Italian Population

¹ Laboratorio di Chimica Clinica e Microbiologia, Azienda Ospedaliera San Paolo, Via di Rudinì 8, 20142 Milan, Italy;
² Clinica Pediatrica, Azienda Ospedaliera San Paolo, Università di Milano, Via di Rudinì 8, 20142 Milan, Italy;
^a author for correspondence: fax 39-0289128221

Gilbert syndrome, a benign unconjugated hyperbilirubinemia without structural liver disease or overt hemolysis, is characterized by episodes of mild intermittent jaundice (1)(2)(3). Gilbert syndrome is the most common inherited variant of hepatic bilirubin metabolism, occurring in 2–12% of the population, and it is often detected in adulthood during routine blood tests. The most consistent feature in Gilbert syndrome is a deficiency in bilirubin glucuronidation, but the metabolism of drugs may also be affected(3).

Recently, the molecular basis of Gilbert syndrome was elucidated and found to result from molecular lesions in one of the isoforms of the UDP-glucuronosyl transferase (UGT-1A) gene. UGT-1A is encoded by the UDG gene complex, which is composed of multiple unique forms of exon 1, each one specific for a single isoenzymes, and four common exons (from two to five) (4). UGT-1A is responsible for bilirubin glucuronidation; the other isoenzymes of the complex are involved in the metabolism of a number of aromatic compounds(5).

The most common genetic alteration of UGT-1A is a TA insertion in the repetitive TATA-box . . . [Full Text of this Article]

References

The following articles in journals at HighWire Press have cited this article:

				E. Costa, E. Vieira, and R. dos Santos The Polymorphism c.-3279T>G in the Phenobarbital-Responsive Enhancer Module of the Bilirubin UDP-Glucuronosyltransferase Gene Is Associated with Gilbert Syndrome Clin. Chem., November 1, 2005; 51(11): 2204 - 2206. [Full Text] [PDF]

				S. D. Zucker, X. Qin, S. D. Rouster, F. Yu, R. M. Green, P. Keshavan, J. Feinberg, and K. E. Sherman Mechanism of indinavir-induced hyperbilirubinemia PNAS, October 12, 2001; (2001) 231140698. [Abstract] [Full Text] [PDF]

				C. Guillemette, I. De Vivo, S. E. Hankinson, C. A. Haiman, D. Spiegelman, D. E. Housman, and D. J. Hunter Association of Genetic Polymorphisms in UGT1A1 with Breast Cancer and Plasma Hormone Levels Cancer Epidemiol. Biomarkers Prev., June 1, 2001; 10(6): 711 - 714. [Abstract] [Full Text] [PDF]

				S. D. Zucker, X. Qin, S. D. Rouster, F. Yu, R. M. Green, P. Keshavan, J. Feinberg, and K. E. Sherman Mechanism of indinavir-induced hyperbilirubinemia PNAS, October 23, 2001; 98(22): 12671 - 12676. [Abstract] [Full Text] [PDF]