Immediate pre-ovulatory administration of 30 mg ulipristal acetate significantly delays follicular rupture.
Summary of "Immediate pre-ovulatory administration of 30 mg ulipristal acetate significantly delays follicular rupture."
BACKGROUND Current methods of hormonal emergency contraception (EC) are ineffective in preventing follicular rupture when administered in the advanced pre-ovulatory phase. This study was designed to determine the capacity of ulipristal acetate (UPA), a selective progesterone receptor modulator developed for EC, to block follicular rupture when administered with a follicle of >/=18 mm. METHODS This was a double-blind, crossover, randomized, placebo-controlled study. Thirty-five women contributed with UPA (30 mg. oral) and a placebo cycle. Serial blood sampling for luteinizing hormone (LH), estradiol and progesterone measurements and follicular monitoring by ultrasound were performed before and for 5 days following treatment. Follicular rupture inhibition was assessed in the overall study population and in subgroups of women stratified by when treatment was administered in relation to LH levels (before the onset of the LH surge, after the onset of the surge but before the LH peak or after the LH peak). RESULTS Follicular rupture failed to occur for at least 5 days following UPA administration in 20/34 cycles [59%; 95% confidence interval (CI) (40.7-75.4%)], whereas rupture took place in all cycles within 5 days of placebo intake. When UPA was administered before the onset of the LH surge, or after the onset but before the LH peak, follicle rupture had not occurred within 5 days in 8/8 (100%) and 11/14 [78.6%; 95% CI (49.2-95.3)] cycles, respectively. In contrast, when UPA was given after the LH peak, follicle rupture inhibition was only observed in 1/12 [8.3%; 95% CI (0.2-38.5)] cycles. CONCLUSIONS This study demonstrates that UPA can significantly delay follicular rupture when given immediately before ovulation. This new generation EC compound could possibly prevent pregnancy when administered in the advanced follicular phase, even if LH levels have already begun to rise, a time when levonorgestrel EC is no longer effective in inhibiting ovulation. NCT01107093: Comparison of CDB-2914 versus placebo in the prevention of follicular rupture post-LH surge.
Affiliation
PROFAMILIA, Nicolas de Ovando & Calle 16, Santo Domingo 10401, Dominican Republic.
Journal Details
This article was published in the following journal.
Name: Human reproduction (Oxford, England)
ISSN: 1460-2350
Pages:
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20634186
- DOI: http://dx.doi.org/10.1093/humrep/deq157
Medical and Biotech [MESH] Definitions
Follicular Phase
The period of the MENSTRUAL CYCLE representing follicular growth, increase in ovarian estrogen (ESTROGENS) production, and epithelial proliferation of the ENDOMETRIUM. Follicular phase begins with the onset of MENSTRUATION and ends with OVULATION.
Acetylesterase
An enzyme that catalyzes the conversion of acetate esters and water to alcohols and acetate. EC 3.1.1.6.
Megestrol Acetate
Megestrol acetate is a progestogen with actions and uses similar to those of the progestogens in general. It also has anti-androgenic properties. It is given by mouth in the palliative treatment or as an adjunct to other therapy in endometrial carcinoma and in breast cancer. Megestrol acetate has been approved to treat anorexia and cachexia. (From Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)
Melengestrol Acetate
A 6-methyl PROGESTERONE acetate with reported glucocorticoid activity and effect on ESTRUS.
Acetate-coa Ligase
An enzyme that catalyzes the formation of CoA derivatives from ATP, acetate, and CoA to form AMP, pyrophosphate, and acetyl CoA. It acts also on propionates and acrylates. EC 6.2.1.1.
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