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Biological Effects of Various Doses of Conjugated Equine Estrogens in Postmenopausal Women^*

Departments of Medicine and Obstetrics and Gynecology, University of California Los Angeles,California 90024; the Medical Services of Wadsworth Veterans Administration Hospital, Los Angeles,California 90073; and Sepulveda Veterans Administration Hospital, Sepulveda, Californi 91343

Address requests for reprints to: Dr. Howard L. Judd, Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, UCLA School of Medicine, Los Angeles, California 90024.

To determine which dosage of estrogen might provide physiological replacement and also avoid possible harmful side effects, 21 postmenopausal women were studied before and after the oral administration of conjugated equine estrogens. The dosages studied were 0.15, 0.30, 0.625, and1.25 mg/day, with each being given for 6 weeks. Fifteen premenopausal women ere also studied, and their values were presumed to reflect normal physiological function

Variable responses of the different biochemical and biological markers of the action of estrogen were observed. Both LH and FS levels showed stepwise decreases with increasing amounts of estrogen, but even 1.25 mg;/day did notsuppress these hormones to the range found in premenopausawomen, suggesting a subphysiological response. The lower dosages of conjugated estrogen had minimal effects on vaginal cytology, withonly the 1.25-mg dose changing the maturation index to values similar to those found in premenopausa subjects. The 0.3-mg dose of conjugated estrogen was the lowest amount that resulted in a significant reduction (P <0.05) of the urinary calcium to creatinine ratio (an index of bone resorption).Liver protein synthesis was the most sensitive parameter to the action of estrogen. Hepatic responses were variable depending on which protein was assessed. These data indicate that the oral administration of conjugated equine estrogens results in inconsistent effects. All doses exerted subphysiological, physiological, and pharmacological responses at the different sites of action.

^* This work was supported in part by USPHD Grants CA-23093, RR-865, and HD-7181 and V.A. Medical Research Funds.

Received January 10, 1980.

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