Emergency contraception

To the Editor: In her recent overview of emergency contraception (November 2012),¹ Dr. Batur wrote that emergency contraception with levonorgestrel (Plan B One-Step) or combined estrogen-progestin-based methods does not cause abortion, noting that it is “unlikely to affect the ability of the embryo to attach to the endometrium.”¹ We disagree. We consider any interruption of human development after fertilization to be abortion (ie, abortifacient).

Recently, Noé et al² found that levonorgestrel was 100% effective in stopping clinical pregnancy when given 1 or 2 days before ovulation. However, previously, Croxatto et al³ noted (through ultrasonography) that levonorgestrel allowed ovulation 88% of the time when given 1 or 2 days before ovulation. Since levonorgestrel’s efficacy is significantly higher than its ability to inhibit ovulation on these days, another mechanism of action must be operant when ovulation does occur, that is, the other 88% of the time. A non-contraceptive action is the most likely explanation by default since the other main effect (ie, thickening of cervical mucus) likely plays little role if levonorgestrel is taken several hours after sexual activity.

Dr. Batur states that levonorgestrel is not an abortion pill because it serves “to enhance the progesterone effect”¹ on the endometrium; however, it causes menstrual bleeding in about 15% of women taking it within 7 days.⁴ In addition, Kesserü et al⁵ noted that the intrauterine pH rose to more than 9 when a low dose was given. This is a 10-fold increase in alkalinity above the normal uterine pH. The pH within the fallopian tubes was not measured, but if a similar rise in pH occurred, it could easily explain how early embryos might die from levonorgestrel.

The medical literature cited above is consistent with the manufacturer’s claim that levonorgestrel “may inhibit implantation,” ⁶ and with the American Congress of Obstetricians and Gynecologists’ statement that “prevention of implantation may be a secondary mechanism of action.”⁷ Physicians and patients should be aware of this important ethical and clinical point.

To the Editor: In her recent overview of emergency contraception (November 2012),¹ Dr. Batur wrote that emergency contraception with levonorgestrel (Plan B One-Step) or combined estrogen-progestin-based methods does not cause abortion, noting that it is “unlikely to affect the ability of the embryo to attach to the endometrium.”¹ We disagree. We consider any interruption of human development after fertilization to be abortion (ie, abortifacient).

Recently, Noé et al² found that levonorgestrel was 100% effective in stopping clinical pregnancy when given 1 or 2 days before ovulation. However, previously, Croxatto et al³ noted (through ultrasonography) that levonorgestrel allowed ovulation 88% of the time when given 1 or 2 days before ovulation. Since levonorgestrel’s efficacy is significantly higher than its ability to inhibit ovulation on these days, another mechanism of action must be operant when ovulation does occur, that is, the other 88% of the time. A non-contraceptive action is the most likely explanation by default since the other main effect (ie, thickening of cervical mucus) likely plays little role if levonorgestrel is taken several hours after sexual activity.

Dr. Batur states that levonorgestrel is not an abortion pill because it serves “to enhance the progesterone effect”¹ on the endometrium; however, it causes menstrual bleeding in about 15% of women taking it within 7 days.⁴ In addition, Kesserü et al⁵ noted that the intrauterine pH rose to more than 9 when a low dose was given. This is a 10-fold increase in alkalinity above the normal uterine pH. The pH within the fallopian tubes was not measured, but if a similar rise in pH occurred, it could easily explain how early embryos might die from levonorgestrel.

The medical literature cited above is consistent with the manufacturer’s claim that levonorgestrel “may inhibit implantation,” ⁶ and with the American Congress of Obstetricians and Gynecologists’ statement that “prevention of implantation may be a secondary mechanism of action.”⁷ Physicians and patients should be aware of this important ethical and clinical point.

To the Editor: In her recent overview of emergency contraception (November 2012),¹ Dr. Batur wrote that emergency contraception with levonorgestrel (Plan B One-Step) or combined estrogen-progestin-based methods does not cause abortion, noting that it is “unlikely to affect the ability of the embryo to attach to the endometrium.”¹ We disagree. We consider any interruption of human development after fertilization to be abortion (ie, abortifacient).

Recently, Noé et al² found that levonorgestrel was 100% effective in stopping clinical pregnancy when given 1 or 2 days before ovulation. However, previously, Croxatto et al³ noted (through ultrasonography) that levonorgestrel allowed ovulation 88% of the time when given 1 or 2 days before ovulation. Since levonorgestrel’s efficacy is significantly higher than its ability to inhibit ovulation on these days, another mechanism of action must be operant when ovulation does occur, that is, the other 88% of the time. A non-contraceptive action is the most likely explanation by default since the other main effect (ie, thickening of cervical mucus) likely plays little role if levonorgestrel is taken several hours after sexual activity.

Dr. Batur states that levonorgestrel is not an abortion pill because it serves “to enhance the progesterone effect”¹ on the endometrium; however, it causes menstrual bleeding in about 15% of women taking it within 7 days.⁴ In addition, Kesserü et al⁵ noted that the intrauterine pH rose to more than 9 when a low dose was given. This is a 10-fold increase in alkalinity above the normal uterine pH. The pH within the fallopian tubes was not measured, but if a similar rise in pH occurred, it could easily explain how early embryos might die from levonorgestrel.

The medical literature cited above is consistent with the manufacturer’s claim that levonorgestrel “may inhibit implantation,” ⁶ and with the American Congress of Obstetricians and Gynecologists’ statement that “prevention of implantation may be a secondary mechanism of action.”⁷ Physicians and patients should be aware of this important ethical and clinical point.