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Stroke. 2003;34:338-341
doi: 10.1161/01.STR.0000054051.88378.25
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(Stroke. 2003;34:338.)
© 2003 American Heart Association, Inc.


Advances in Stroke 2002

Estrogen and Stroke

A Balanced Analysis

Patricia D. Hurn, PhD Lawrence M. Brass, MD

From the Department of Anesthesiology and Critical Care Medicine, Johns Hopkins School of Medicine (P.D.H.), Baltimore, Md; the Departments of Neurology and Epidemiology & Public Health, Yale University School of Medicine (L.M.B.), New Haven, Conn; and the Neurology Service of VA Connecticut Healthcare System (L.M.B.), West Haven, Conn.

Correspondence to Patricia D. Hurn, PhD, Blalock 1404, Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21287. E-mail phurn@jhmi.edu


Key Words: cerebral ischemia • estrogen • ischemic stroke • neuroprotection • stroke risk


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

Aging women sustain a large burden for stroke, an observation frequently overlooked in our popularized view of cancer as the killer of women. Accordingly, potential benefits and hazards of hormone replacement therapy (HRT) are of increasing interest to female patients at risk for stroke and cerebrovascular disease. Estrogen has been particularly well studied in animal and cell injury models of cerebral ischemia with nearly uniform favorable results, ie, cell salvage from ischemic death pathways. Nevertheless, our ability to translate these favorable data from the bench into positive clinical trials has been quite limited. Furthermore, recent data from large, randomized, clinical trials question the use of HRT for either the primary or secondary prevention of coronary heart disease and stroke. This review will evaluate experimental and clinical evidence for estrogen’s efficacy, or lack thereof, and mechanisms of action in cerebral ischemia and stroke.

Estrogen Appears Strongly Neuroprotective in Stroke Models

Animal studies clearly indicate that biologic sex and endogenous sex steroids influence experimental stroke outcome. Histological damage is less in female animals than in age-matched males after focal cerebral ischemia, and the source of this protection is linked to female reproductive steroids.1–3 Furthermore, emerging data suggest that molecular mechanisms of ischemic damage may not necessarily impact identically in male and female brains. For example, ischemic outcome in transgenic mouse strains can be sex-dependent, even when the deleted (or overexpressed) gene is not linked to reproduction.4

Estrogen has been widely shown to acutely protect brain from experimental stroke.5–8 These observations have been consistent across animal models, breeder source, and . . . [Full Text of this Article]




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