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June 26, 1996

Estrogen Replacement Therapy and Endometrial Hyperplasia

Author Affiliations

University of Cincinnati Medical Center Cincinnati, Ohio

JAMA. 1996;275(24):1880. doi:10.1001/jama.1996.03530480022022

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 17α-dihydroequilin, equilin, equilenin amounting to nearly 51%), and