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  Vol. 275 No. 24, June 26, 1996 TABLE OF CONTENTS
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Estrogen Replacement Therapy and Endometrial Hyperplasia

M. T. R. Subbiah, PhD
University of Cincinnati Medical Center Cincinnati, Ohio

JAMA. 1996;275(24):1880.

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

To the Editor.

—The Writing Group for the Postmenopausal Estrogen/Progestin Intervention (PEPI) trial1 recently reported on the development of endometrial hyperplasia as influenced by conjugated equine estrogens (CEE). Although estrogen replacement therapy is widely advocated as a means to combat symptoms of menopause and reduce the risk of osteoporosis and heart disease, increase in endometrial cancer continues to be a major concern.

In many of the human studies, including the above-mentioned PEPI trial, CEE is the predominant form of estrogen used. One of the most ignored (but vital) facts that was left out of the discussion is that CEE represents a mixture of conjugated estrogens isolated from the urine of pregnant mares, which contains at least 7 major components.2,3 Among these, estrone sulfate is the predominant estrogen (about 45%) with a significant amount of ring B unsaturated equine estrogens (predominantly 17{alpha}-dihydroequilin, equilin, equilenin amounting to nearly 51%), and . . . [Full Text PDF of this Article]



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