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  Vol. 164 No. 22, Dec 13/27, 2004 TABLE OF CONTENTS
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 •Asthma
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Postmenopausal Asthma: The Estradiol 11{beta}-Hydroxysteroid Dehydrogenase Connection

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Barr and colleagues1 reported that postmenopausal female hormone therapy is associated with an increased rate of onset of asthma. They noted that the incidence of asthma usually decreases with the onset of menopause and that estrogens may exert proinflammatory effects.

In their discussion, their comments on common proinflammatory mechanisms that activate asthma failed to include the possibility that a decrease in the anti-inflammatory protection provided by cortisol might allow asthma to develop. Cortisol is an extremely powerful anti-inflammatory agent that may be protective against the development of chronic inflammation.2

Until recently, plasma cortisol concentrations were considered to provide a clinically relevant measure of cortisol availability and adequacy. It is now clear that intracellular cortisol concentrations are more important and are regulated, in a tissue-specific manner, by the 11{beta}-hydroxysteroid dehydrogenase type I isoenzyme.3 Furthermore, it has been demonstrated that estrogen is capable of inhibiting the activity of this enzyme, thereby . . . [Full Text of this Article]


AUTHOR INFORMATION
Paul G. Cohen, MD; John M. Holbrook, PhD


RELATED ARTICLE

Prospective Study of Postmenopausal Hormone Use and Newly Diagnosed Asthma and Chronic Obstructive Pulmonary Disease
R. Graham Barr, Catherine C. Wentowski, Francine Grodstein, Samuel C. Somers, Meir J. Stampfer, Joel Schwartz, Frank E. Speizer, and Carlos A. Camargo, Jr
Arch Intern Med. 2004;164(4):379-386.
ABSTRACT | FULL TEXT  






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