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Clinical Chemistry 49: 1180-1181, 2003; 10.1373/49.7.1180
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(Clinical Chemistry. 2003;49:1180-1181.)
© 2003 American Association for Clinical Chemistry, Inc.

Technical Briefs

UGT1A1*28 Allele and Coronary Heart Disease: The Rotterdam Study

Piter J. Bosma1,a, Irene M. van der Meer2, Conny T. Bakker1, Albert Hofman1, Marianne Paul-Abrahamse1 and Jacqueline C. Witteman2

1 Liver Center, Academic Medical Center, Meibergdreef 9, 1105AZ Amsterdam, The Netherlands

2 Department of Epidemiology & Biostatistics, Erasmus MC, University Medical Center, Rotterdam, PO Box 1738, 3000DR Rotterdam, The Netherlands

aauthor for correspondence: fax 31-20-5669190, e-mail P.J.Bosma@amc.uva.nl

The first 20% of the full text of this article appears below.

Oxidative reactions, such as lipid oxidation and the formation of oxygen radicals, are involved in the pathophysiology of arteriosclerosis and coronary heart disease (CHD) (1). Bilirubin, the metabolic waste product of heme degradation, is an endogenous antioxidant and could thus have a protective effect against CHD (2). In vitro, conjugated and unconjugated bilirubin are scavengers of peroxyl radicals and are able to protect human LDL against peroxidation (3)(4). In vivo, increased serum bilirubin was shown to produce an enhanced antioxidant status of serum (5). In addition, an association between low serum bilirubin and the risk of CHD has been observed in several studies (6)(7)(8).

A recent family heart study inferred the existence of a major gene for high bilirubin concentrations that may protect against CHD (9). A likely candidate gene responsible for high serum bilirubin is the gene encoding the hepatic enzyme bilirubin UDP-glucuronosyltransferase (UGT1A1). Glucuronidation is an essential step in the biliary excretion of bilirubin, and decreased UGT1A1 activity leads to increased serum concentrations of unconjugated bilirubin (10). A common etiology of decreased UGT1A1 activity is the insertion of a TA in the TATAA box in the promoter region of the UGT1A1 gene (11). Transcription of the UGT1A1 gene is fivefold lower in individuals with this allele, designated UGT1A1*28.

Individuals homozygous for the UGT1A1*28 allele (genotype 7/7) have mildly increased serum bilirubin compared with heterozygotes (genotype 6/7) and homozygous wild-type individuals (genotype 6/6) (12). In Caucasian populations, the frequency of individuals homozygous for this allele is 10–16% (11)(12). This is close . . . [Full Text of this Article]




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