Ulipristal Acetate (ella)

INTRODUCTION In the U.S., it is estimated that onehalf of the six million pregnancies that occur each year are unplanned or un expected.1 Despite the widespread of use of various contraceptive methods, including hormonal contraceptive tablets and condoms, these methods remain imperfect. Inadequate contraceptive use or failure of a contraceptive method, in addition to unprotected sexual intercourse, may contribute to the incidence of un intended pregnancies. According to the Centers for Disease Control and Prevention (CDC), an estimated 1.21 million abortions were reported in 2005 in the U.S.2 Easier access to postcoital or emergency contraception (EC) might help to reduce the incidence of un intended pregnancy and abortion. Recent data indicate that women are increasingly seeking EC use, with 4% reporting having used it at least once in 2002 and 10% reporting use between 2006 and 2008.3 A variety of EC methods, including oral medications and a copper intrauterine device (IUD)— which may be inserted up to five days after unprotected intercourse—are currently available. Although sometimes referred to as the “morning-after pill,” this moniker is misleading; the hormonal progesterone receptors to produce an anti-progesterone contraceptive effect on the ovary (by suppressing or delaying ovulation) and on the endometrium (by decreasing endometrial thickness). These effects vary according to the timing of drug administration during the menstrual cycle.10 Progesterone is crucial for pregnancy to occur and for sustaining the pregnancy by preparing the endometrium for implantation of the fertilized egg.10 Ulipristal acetate binds to the progesterone receptor and blocks the hormone’s effects. To achieve improved specificity for the progesterone receptor, ulipristal acetate was developed to be a derivative of 19-norprogesterone. It possesses the ability to inhibit or delay ovulation, ultimately preventing pregnancy within 120 hours of unprotected intercourse or suspected contraceptive failure. The medication’s effects may vary, depending on the dose and phase of the menstrual cycle during which it is taken.11 Administering ulipristal acetate before ovulation causes delayed follicle development and release, probably a result of suppression of estradiol levels. If the EC drug is taken during the LH peak, follicular rupture and ovum release may also be delayed.11 During the latter part of the menstrual cycle, ulipristal acetate’s effect may be attributed to its ability to decrease endometrial thickness.6 In addition to its effects on human progesterone receptors, ulipristal acetate binds to glucocorticoid and androgen receptors. However, its capacity as an antagonist in binding to these receptors is markedly lower than its anti-progestational activity. Anti-glucocorticoid and anti-androgen activities were observed at doses 50-fold greater than that necessary for an anti-progestin effect, indicating that ulipristal acetate is a progesterone receptor modulator with reduced anti-glucocorticoid activity.11 Ms. Kim is a student at the Ernest Mario School of Pharmacy, Rutgers University, in Piscataway, N.J. Dr. Bridgeman is a Clinical Assistant Professor at the Ernest Mario School of Pharmacy, Rutgers University, and an Internal Medicine Clinical Pharmacist at Capital Health Regional Medical Center in Trenton, N.J. Drug Forecast is a regular column coordinated by Alan Caspi, PhD, PharmD, MBA, President of Caspi & Associates in New York, N.Y. Andrea Kim, PharmD Candidate; and Mary Barna Bridgeman, PharmD, BCPS