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(Hypertension. 2003;42:e3.)
© 2003 American Heart Association, Inc.

Letters to the Editor

Glucocorticoid Receptor Gene and Coronary Artery Disease: Right Idea, Wrong Gene Variant?

Department of Clinical Chemistry, Sahlgrenska University Hospital, Göteborg, Sweden

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Recent data reported by Lin et al¹ suggest that coronary artery disease (CAD) is associated with an Asn363Ser variant in exon 2 of the glucocorticoid receptor gene (GRL). The study is based on the notion that a dysfunctional glucocorticoid receptor may add to the adverse health effects of excessive cortisol concentrations.

In a previous study, comprising Anglo-Celtic descent with a strong hereditability for hypertension and formerly designed to test the relationship between GRL and essential hypertension, the authors found an association between the Ser363 variant and elevated body mass index (BMI).² However, no association or linkage with hypertension was detected.³ This lack of effect on blood pressure has been reported previously in a Dutch cohort.⁴

The authors fail to provide valuable pieces of information regarding previously published observations. The fact is that the only studies indicating an association between the Ser363 variant and obesity, measured as BMI, is that of Lin et al² and Huizenga et al.⁴ In the referenced study of the Newcastle Heart Project,⁵ a significant association of the Ser allele was detected with increased waist-to-hip ratio (WHR) and not BMI in white men. To see an association with WHR in this report the authors needed to correct for a number of other factors that associate with central obesity, hence the multivariate approach (Christopher P.F. Redfern, personal communication, 2001). More importantly, however, is that a majority of studies indicates that the ATT to GTT point variation in exon 2 of the GRL is . . . [Full Text of this Article]

Brian J. Morris; Ruby C.Y. Lin

Basic & Clinical Genomics Laboratory, School of Medical Sciences, and Institute for Biomedical Research, The University of Sydney, Sydney, Australia

Xing Li Wang

Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas, Cardiovascular Genetics Laboratory, Prince of Wales Hospital, Centre for Thrombosis and Vascular Research, University of New South Wales, Sydney, Australia