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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.
- Batur P. Emergency contraception: Separating fact from fiction. Clev Clin J Med 2012; 79:771–776.
- Noé G, Croxatto HB, Salvatierra AM, et al. Contraceptive efficacy of emergency contraception with levonorgestrel given before or after ovulation. Contraception 2011; 84:486–492.
- Croxatto HB, Brache V, Pavez M, et al. Pituitary-ovarian function following the standard levonorgestrel emergency contraceptive dose or a single 0.75-mg dose given on the days preceding ovulation. Contraception 2004; 70:442–450.
- Gainer E, Kenfack B, Mboudou E, Doh AS, Bouyer J. Menstrual bleeding patterns following levonorgestrel emergency contraception. Contraception 2006; 74:118–124.
- Kesserü E, Garmendia F, Westphal N, Parada J. The hormonal and peripheral effects of d-norgestrel in postcoital contraception. Contraception 1974; 10:411–424.
- Teva Women’s Health Inc. Plan B One-Step product information. www.planbonestep.com/pdf/PlanBOneStep-FullProductInformation.pdf. Accessed January 10, 2013.
- American College of Obstetricians and Gynecologists. Frequently asked question 114. www.acog.org/~/media/For%20Patients/faz/114.pdf?dmc=1&ts=20121127T11830130312.
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.
- Batur P. Emergency contraception: Separating fact from fiction. Clev Clin J Med 2012; 79:771–776.
- Noé G, Croxatto HB, Salvatierra AM, et al. Contraceptive efficacy of emergency contraception with levonorgestrel given before or after ovulation. Contraception 2011; 84:486–492.
- Croxatto HB, Brache V, Pavez M, et al. Pituitary-ovarian function following the standard levonorgestrel emergency contraceptive dose or a single 0.75-mg dose given on the days preceding ovulation. Contraception 2004; 70:442–450.
- Gainer E, Kenfack B, Mboudou E, Doh AS, Bouyer J. Menstrual bleeding patterns following levonorgestrel emergency contraception. Contraception 2006; 74:118–124.
- Kesserü E, Garmendia F, Westphal N, Parada J. The hormonal and peripheral effects of d-norgestrel in postcoital contraception. Contraception 1974; 10:411–424.
- Teva Women’s Health Inc. Plan B One-Step product information. www.planbonestep.com/pdf/PlanBOneStep-FullProductInformation.pdf. Accessed January 10, 2013.
- American College of Obstetricians and Gynecologists. Frequently asked question 114. www.acog.org/~/media/For%20Patients/faz/114.pdf?dmc=1&ts=20121127T11830130312.
- Batur P. Emergency contraception: Separating fact from fiction. Clev Clin J Med 2012; 79:771–776.
- Noé G, Croxatto HB, Salvatierra AM, et al. Contraceptive efficacy of emergency contraception with levonorgestrel given before or after ovulation. Contraception 2011; 84:486–492.
- Croxatto HB, Brache V, Pavez M, et al. Pituitary-ovarian function following the standard levonorgestrel emergency contraceptive dose or a single 0.75-mg dose given on the days preceding ovulation. Contraception 2004; 70:442–450.
- Gainer E, Kenfack B, Mboudou E, Doh AS, Bouyer J. Menstrual bleeding patterns following levonorgestrel emergency contraception. Contraception 2006; 74:118–124.
- Kesserü E, Garmendia F, Westphal N, Parada J. The hormonal and peripheral effects of d-norgestrel in postcoital contraception. Contraception 1974; 10:411–424.
- Teva Women’s Health Inc. Plan B One-Step product information. www.planbonestep.com/pdf/PlanBOneStep-FullProductInformation.pdf. Accessed January 10, 2013.
- American College of Obstetricians and Gynecologists. Frequently asked question 114. www.acog.org/~/media/For%20Patients/faz/114.pdf?dmc=1&ts=20121127T11830130312.
Menstrual manipulation
To the Editor: In the article, “Menstrual manipulation: Options for suppressing the cycle,”1 the authors described advantages and disadvantages of various hormone-based methods of menstrual manipulation, including prolonged use of oral contraceptives. We believe the authors underemphasized the risks associated with oral contraceptives. Blood clots, stroke, and death are often included in print and television ads by law firms recruiting patients harmed by these drugs. In addition, the authors failed to mention the risk of premenopausal breast cancer due to oral contraceptives, which are now classified as group 1 carcinogens by the World Health Organization.2
In October 2006, we published the most current meta-analysis to date regarding oral contraceptive use and the risk of premenopausal breast cancer.3 We found that 21 out of 23 studies showed a positive trend or positive risk for premenopausal breast cancer with oral contraceptive use prior to first-term pregnancy. This resulted in a highly statistically significant cumulative risk of 44% (ie, odds ratio 1.44, 95% confidence interval 1.24–1.68). Our meta-analysis remains the most recent study in this area and updates the Oxford pooled analysis,4 which relied on older studies with older women (two-thirds of whom were over age 45).
A more recent collaborative study coauthored by investigators from the National Cancer Institute, the Hutchinson Cancer Research Center, and the University of Washington includes oral contraceptives in the list of risk factors for breast cancer in younger women.5 We ask your readers to consider that patients are entitled to know about this important risk factor before making a decision regarding hormonal menstrual manipulation.
- Hicks CW, Rome ES. Menstrual manipulation: options for suppressing the cycle. Clev Clin J Med 2010; 77:445–453.
- Cogliano V, Grosse Y, Baan R, et al; WHO International Agency for Research on Cancer. Carcinogenicity of combined oestrogen-progestagen contraceptives and menopausal treatment. Lancet Oncol 2005; 6:552–553.
- Kahlenborn C, Modugno F, Potter DM, Severs WB. Oral contraceptive use as a risk factor for premenopausal breast cancer: a meta-analysis. Mayo Clin Proc 2006; 81:1290–1302.
- Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: further results. Contraception 1996; 54(3 suppl):1S–106S.
- Dolle JM, Daling JR, White E, et al. Risk factors of triple-negative breast cancer in women under the age of 45 years. Cancer Epidemiol Biomarkers Prev 2009; 18:1157–1166.
To the Editor: In the article, “Menstrual manipulation: Options for suppressing the cycle,”1 the authors described advantages and disadvantages of various hormone-based methods of menstrual manipulation, including prolonged use of oral contraceptives. We believe the authors underemphasized the risks associated with oral contraceptives. Blood clots, stroke, and death are often included in print and television ads by law firms recruiting patients harmed by these drugs. In addition, the authors failed to mention the risk of premenopausal breast cancer due to oral contraceptives, which are now classified as group 1 carcinogens by the World Health Organization.2
In October 2006, we published the most current meta-analysis to date regarding oral contraceptive use and the risk of premenopausal breast cancer.3 We found that 21 out of 23 studies showed a positive trend or positive risk for premenopausal breast cancer with oral contraceptive use prior to first-term pregnancy. This resulted in a highly statistically significant cumulative risk of 44% (ie, odds ratio 1.44, 95% confidence interval 1.24–1.68). Our meta-analysis remains the most recent study in this area and updates the Oxford pooled analysis,4 which relied on older studies with older women (two-thirds of whom were over age 45).
A more recent collaborative study coauthored by investigators from the National Cancer Institute, the Hutchinson Cancer Research Center, and the University of Washington includes oral contraceptives in the list of risk factors for breast cancer in younger women.5 We ask your readers to consider that patients are entitled to know about this important risk factor before making a decision regarding hormonal menstrual manipulation.
To the Editor: In the article, “Menstrual manipulation: Options for suppressing the cycle,”1 the authors described advantages and disadvantages of various hormone-based methods of menstrual manipulation, including prolonged use of oral contraceptives. We believe the authors underemphasized the risks associated with oral contraceptives. Blood clots, stroke, and death are often included in print and television ads by law firms recruiting patients harmed by these drugs. In addition, the authors failed to mention the risk of premenopausal breast cancer due to oral contraceptives, which are now classified as group 1 carcinogens by the World Health Organization.2
In October 2006, we published the most current meta-analysis to date regarding oral contraceptive use and the risk of premenopausal breast cancer.3 We found that 21 out of 23 studies showed a positive trend or positive risk for premenopausal breast cancer with oral contraceptive use prior to first-term pregnancy. This resulted in a highly statistically significant cumulative risk of 44% (ie, odds ratio 1.44, 95% confidence interval 1.24–1.68). Our meta-analysis remains the most recent study in this area and updates the Oxford pooled analysis,4 which relied on older studies with older women (two-thirds of whom were over age 45).
A more recent collaborative study coauthored by investigators from the National Cancer Institute, the Hutchinson Cancer Research Center, and the University of Washington includes oral contraceptives in the list of risk factors for breast cancer in younger women.5 We ask your readers to consider that patients are entitled to know about this important risk factor before making a decision regarding hormonal menstrual manipulation.
- Hicks CW, Rome ES. Menstrual manipulation: options for suppressing the cycle. Clev Clin J Med 2010; 77:445–453.
- Cogliano V, Grosse Y, Baan R, et al; WHO International Agency for Research on Cancer. Carcinogenicity of combined oestrogen-progestagen contraceptives and menopausal treatment. Lancet Oncol 2005; 6:552–553.
- Kahlenborn C, Modugno F, Potter DM, Severs WB. Oral contraceptive use as a risk factor for premenopausal breast cancer: a meta-analysis. Mayo Clin Proc 2006; 81:1290–1302.
- Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: further results. Contraception 1996; 54(3 suppl):1S–106S.
- Dolle JM, Daling JR, White E, et al. Risk factors of triple-negative breast cancer in women under the age of 45 years. Cancer Epidemiol Biomarkers Prev 2009; 18:1157–1166.
- Hicks CW, Rome ES. Menstrual manipulation: options for suppressing the cycle. Clev Clin J Med 2010; 77:445–453.
- Cogliano V, Grosse Y, Baan R, et al; WHO International Agency for Research on Cancer. Carcinogenicity of combined oestrogen-progestagen contraceptives and menopausal treatment. Lancet Oncol 2005; 6:552–553.
- Kahlenborn C, Modugno F, Potter DM, Severs WB. Oral contraceptive use as a risk factor for premenopausal breast cancer: a meta-analysis. Mayo Clin Proc 2006; 81:1290–1302.
- Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormonal contraceptives: further results. Contraception 1996; 54(3 suppl):1S–106S.
- Dolle JM, Daling JR, White E, et al. Risk factors of triple-negative breast cancer in women under the age of 45 years. Cancer Epidemiol Biomarkers Prev 2009; 18:1157–1166.