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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1741.)
© 2004 American Heart Association, Inc.

Editorials

Estrogen and HDL

All that Glitters Is not Gold

David M. Herrington; John S. Parks

From the Department of Internal Medicine/Cardiology, Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to David Herrington, Department of Internal Medicine/Cardiology, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1040. E-mail dherring@wfubmc.edu

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

Since the initial report of the Heart and Estrogen/Progestin Replacement Study (HERS) in 1998, the medical community has struggled to understand the unexpected findings from a series of randomized clinical trials that failed to show a beneficial effect of postmenopausal hormone therapy on risk for cardiovascular events.^1–3 One of the uniformly perplexing features of these trials was the lack of a cardiovascular benefit despite favorable changes in many of the intermediate end points that were previously thought to insure a beneficial effect of estrogen. Chief among these intermediate end points was high density lipoprotein (HDL) cholesterol, which was significantly increased in all of the clinical trials, but whose elevation was apparently not capable of imparting a corresponding reduction in cardiovascular risk. This observation led to speculation that the presumed favorable effects of raising HDL were diminished by other, previously unrecognized, adverse effects. A leading candidate was a proinflammatory effect of estrogen suggested by estrogen induced increases in C-reactive protein (CRP) and other hepatically-derived inflammation proteins. In most discussions, the impact of oral estrogen on HDL and its potential proinflammatory effect were considered separate but offsetting effects with respect to cardiovascular risk.

See pages 1866 and e164

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Abbas et al⁴ present new data suggesting that these two effects of estrogen, elevations in HDL without accompanying cardiovascular benefit and increased expression of inflammation proteins, may be more closely linked than previously thought. In a small crossover design clinical trial, they demonstrate that . . . [Full Text of this Article]

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