The mechanism of ovulation inhibition by triamcinolone acetonide.

doi:10.1210/JCEM-46-1-8

Paper

The mechanism of ovulation inhibition by triamcinolone acetonide.

Published 1978 · G. Cunningham, J. Goldzieher, A. de la Peña

The Journal of clinical endocrinology and metabolism

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43

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1

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Abstract

A single dose of 25 mg triamcinolone acetonide, when given on day 1 or 2 of the menstrual cycle, inhibits ovulation. To examine the mechanism of this action, daily determinations of plasm FSH, LH, estrone plus estradiol (E1 + E2), and progestins were performed. Some subjects also received a single dose of LH-RH or hCG on cycle day 15 or clomiphene citrate on days 5-9. Triamcinolone acetonide itself caused variable suppression of plasma estrogens, loss of the mid-cycle gonadotropin surge, and a deficient or absent rise in plasma progestins. Impaired secretion of estrogen did not seem to be due to low gonadotropin levels. FSH and LH responses to LH-RH were adequate in relation to prevailing estrogen levels. Four of six women treated with clomiphene responded with plasma progestin levels which exceed 8 ng/ml. Triamcinolone acetonide seems to affect the hypothalamic-pituitary-ovarian axis mainly by hypothalamic suppression and possibly by a direct effect on the ovary as well.

Non-RCT

Study Snapshot

Triamcinolone acetonide inhibits ovulation mainly through hypothalamic suppression and possibly by directly affecting the ovary.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

The mechanism of ovulation inhibition by triamcinolone acetonide.

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References

Current status of estrogen and progesterone receptors in breast cancer

Progesterone receptor (PgR) is a promising marker for hormonal responsiveness in breast cancer, with a higher response rate to endocrine therapy when both estrogen and progesterone receptors are present in the tumor.

Biological effects of a new and potent progestagen. A clinical study.

Org 2969, a new synthetic progestagen, led to anovulatory cycles in healthy menstruating women, with no significant side effects observed.

The effect of medroxyprogesterone acetate on the pituitary-adrenal axis.

Medroxyprogesterone acetate (MPA) reduces cortisol levels and suppresses adrenal function, likely through negative feedback on the hypothalamus or pituitary.

Inhibition of the positive feedback of oestradiol during treatment with subcutaneous implants of d-norgestrel.

Subcutaneous implants of d-norgestrel suppress ovulation and block positive feedback on LH release, but do not affect negative feedback.

Strength-duration characteristics of estrogen effects on gonadotropin response to gonadotropin-releasing hormone in women. II. Effects of varying concentrations of estradiol.

Estradiol injections at various concentrations can significantly enhance the gonadotropin response to synthetic gonadotropin-releasing hormone in women.

Citations

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