These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The effects of progesterone and progestins on endometrial proliferation.
    Author: Moyer DL, Felix JC.
    Journal: Contraception; 1998 Jun; 57(6):399-403. PubMed ID: 9693400.
    Abstract:
    A total of 99 premenopausal and 27 postmenopausal women were evaluated to determine the quantity of glandular proliferation resulting from progestin inhibition of estrogen-primed subjects and of subjects without hormonal stimulation. Endometrial glandular proliferation rates were determined by using mitosis counts, proliferating-cell nuclear antigen (PCNA), and nuclear cyclin (MIB1) immunocytological staining. The endometria of normally cycling premenopausal women, of women who received a synthetic progestin, and of untreated postmenopausal women were studied. In untreated normally cycling premenopausal women, the proliferation of the glandular epithelium was increased during the follicular phase and decreased during the luteal phase. Premenopausal women receiving a synthetic progestin and untreated postmenopausal women who were not estrogen-primed showed minimal epithelial proliferation. Endometrial glandular proliferation is inhibited by endogenous progesterone in premenopausal women. Endometrial proliferation is markedly reduced in premenopausal women receiving a synthetic progestin and in untreated postmenopausal women. Use of micronized progesterone or a synthetic progestin has been shown to counter the proliferative effect of estrogen on the endometrium in pre- and postmenopausal women. The present study measured endometrial glandular proliferation rates in 99 pre- and 27 postmenopausal US women. Determinations were based on mitosis counts and both proliferating cell nuclear antigen and nuclear cyclin immunocytologic staining of endometrial tissue. In the untreated, normally cycling premenopausal subjects, glandular epithelial proliferation increased during the follicular phase and decreased during the luteal phase. Premenopausal women who received a synthetic progestin and untreated postmenopausal women who were not estrogen-primed showed minimal epithelial proliferation. The mean mitosis rate of proliferative phase glands was 12.3 compared with 1.6 and 0.01 after administration of the oral contraceptives norethindrone or norethynodrel, respectively. Among premenopausal women, the intensity of the stromal pseudodecidualization and inhibition of glandular development was greatest in those receiving monthly medroxyprogesterone acetate injections. The combination of progestin potency, dosage, and duration determined the mitoses, stroma, and glands that were present in the three groups of subjects. The methods used in this study may be of use in determining optimal dosages of exogenous progestins in women who are receiving hormone replacement therapy and the potential exists for predicting adverse endometrial responses to progestational therapy.
    [Abstract] [Full Text] [Related] [New Search]