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Howard Judd, MD
Olive View—UCLA Medical Center Sylmar, Calif

JAMA. 1996;275(24):1880-1881.

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

In Reply.

—We thank Drs Subbiah and Tsang for their thoughtful letters about our article. Subbiah indicates a need for evaluating the biologic effects of the various estrogen components in CEEs and we would welcome and encourage such studies. Regarding the impact that CEE had on the endometrium, other estrogenic compounds also have been shown to promote the development of endometrial hyperplasia. These include piperazine estrone sulfate, estradiol valerate, estriol hemisuccinate, and transdermal estradiol.^1-3 Even the so-called antiestrogen, tamoxifen, appears to promote the development of endometrial hyperplasia.⁴ Thus, the promotion of endometrial overgrowth is likely a generic response to the class of steroids called estrogens and not to any one single estrogen.

Tsang questions if it is possible to predict which women with endometrial hyperplasia will revert to normal with progestin therapy and suggests the measurement of ER/PRs may predict the response of hyperplasia to progestin therapy. We . . . [Full Text PDF of this Article]

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