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Letters to the Editor

Primary Care April 2003

The Resident Conundrum

To the Editor:

Dr Ronald Burkman’s editorial in the recent The Female Patient (Residents and Decreased Duty Hours. 2003;28(2):8) was outstanding. It perfectly summarizes the conundrum to which we all face: Is it a job or a profession? The more experienced of us (I refuse to say older), still feel it is a profession and we have pride in our work. I am not sure that same attitude is similar among our trainees.

Like Dr Burkman stated it, only time will tell.

Edward C. Grendys, Jr, MD
Tampa, Fla

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Misunderstood Findings?

To the Editor:

I read with great interest Dr Birge’s response to question 3 in your January 2003 issue (Birge SJ. The faculty speaks: questions & answers. The Female Patient. 2003;28(2 suppl):21). I have a few comments. First, the statement that Dr Fisher¹ found a doubling of the occurrence of breast cancer in an additional 5 years is not what I read. "Through 7 years after reassignment to either placebo or continued tamoxifen, a slight advantage was observed in patients who discontinued tamoxifen relative to those who continued to receive it: DFS = 82% vs 78%, RFS = 94% vs 91%." Where is the 80% increase in mortality? Next Birge states that Jordan² gave raloxifene to women who had been on tamoxifen. My reading of Jordan and O’Regan’s³ work was that they used breast cancer cells inserted into mice and then gave the mice estrogen to stimulate growth followed by tamoxifen and raloxifene. Hardly an evidence-based meaningful study. To glibly state that raloxifene taken for the long term may increase a woman’s risk of breast cancer is at best a premature and at worst criminal.

Kenneth A. Baer, MD
Miami, Fla

References

1. Fisher B, Dignam J, Bryant J, et al. Five versus more than five years of tamoxifen therapy for breast cancer patients with negative lymph nodes and estrogen receptor-positive tumors. J Nat Cancer Inst. 1988;88: 1529-1542.
2. Jordan VC, Gapstur S, Morrow S. Selective estrogen receptor modulation and reduction in risk of breast cancer, osteoporosis, and coronary heart disease. J Nat Cancer Inst. 2001;93(19):1449-1457.
3. O’Regan RM, Gajdos C, Dardes RC, et al. Effects of raloxifene after tamoxifen on breast and endometrial tumor growth in athymic mice. J Natl Cancer Inst. 2002 Feb 20;94(4):274-83

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The author responds

The remarks of Dr Baer are appreciated. However, after reviewing the article by Fisher et al,¹ I was unable to find the statement quoted. It would appear that Dr Baer intended to quote the statement on page 1,535 of the Fisher article: "through 4 years following the second randomization (to either placebo or additional 5 years of tamoxifen), the DFS (disease free survival) of patients who switched from tamoxifen to placebo was 92% compared to 86% for those who continued to receive tamoxifen (p=0.003)." The authors go on to state (p 1535-1536) that the "average annual recurrence rate per 1,000 patients among the tamoxifen-treated women in the second randomization was 35.4, for those who received the placebo, it was 19.3." With respect to mortality, Fisher et al indicate on page 1,537 that those treated with tamoxifen for an additional 5 years experienced 25 deaths compared to 14 deaths in the placebo group–a 79% (to be more exact) increase in mortality with the continuation of tamoxifen. I would not characterize these differences as "slight."

With respect to raloxifene’s effects on breast cancer, Jordan et al,² page 1,454, write: "Tamoxifen-stimulated breast cancer is well recognized (in patients) and provides the rationale for stopping tamoxifen therapy at 5 years. Raloxifene has been shown to promote the growth of tamoxifen-stimulated tumors in the laboratory raising concern about its use (clinically)." The US Preventive Services Task Force has recommended that both tamoxifen and raloxifene not be used to prevent breast cancer in women at average risk of breast cancer and expressed concerns about their use in high risk patients.³

I agree with Dr Baer that we should practice evidenced-based medicine. Unfortunately, the only evidence that we have to guide us is that long-term raloxifene therapy may increase the incidence of and mortality from breast cancer.

Stanley J. Birge, MD
Washington University School of Medicine
St. Louis, Mo

References

1. Fisher B, Dignam J, Bryant J, et al. Five versus more than five years of tamoxifen therapy for breast cancer patients with negative lymph nodes and estrogen receptor positive tumors. J Natl Cancer Inst. 1996;88:1529-1542.
2. Jordan VC, Gapstur S, Morrow M. Selective estrogen receptor modulation and reduction in risk of breast cancer, osteoporosis, and coronary heart disease. J Natl Cancer Inst. 2001;93:1449-1457.
3. US Preventive Services Task Force. Chemoprevention of breast cancer: Recommendations and rationale. Ann Internal Med.2002;137:56-58.

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To the Editor:

I am writing in regarding the article "What’s New in Contraception" by Dr Heather Paladine, which appeared in the February 2003 Primary Care Edition of The Female Patient. Dr Paladine presents new methods of contraception. I was sadly disappointed when natural family planning was not mentioned as a viable alternative to pharmacologic methods. This is not the old method known as rhythm, which was not as effective as desired. Natural family planning is a scientific method that requires specialized training and has an effectiveness, when correctly done, that rivals any pharmacological means of contraception.

A second disappointment is regarding the advantages and disadvantages of various contraceptives listed. There are a large number of patients who regard abortion as a significant ethical issue. Nowhere in the article could I find mention of both oral contraceptives and intrauterine devices as being potentially abortifacient. This information would prove valuable to a sizeable number of patients.

Joseph B. Szgalsky, MD FAAFP
Woodbury, NJ

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The author responds

I agree with Dr Szgalsky that natural family planning (NFP) is an underused form of contraception that can be very effective with proper patient selection and training. However, my intent was not to present an exhaustive review of all methods of contraception, but rather to update clinicians on new methods that have become available in the past few years. Scientific research into the Billings ovulation method of natural family planning, an effective and commonly used form of NFP, dates back to the 1970s,¹ and NFP methods have been used prior to these studies as well. Clinicians interested in teaching NFP and fertility awareness to their patients are encouraged to seek additional training; the methods can be complex and time-intensive to teach.

The literature does not support the theory that oral contraceptives or intrauterine devices act as abortifacients. The primary mechanism of action of IUDs is to interfere with sperm motility. Progesterone-containing IUDs also result in thickening of the cervical mucus and thinning of the endometrium. A 1985 study by Segal et al² found no positive HCG levels in IUD users over a one month period, compared with two positive results in a group of 15 women trying to become pregnant. A similar study by Wilcox et al³ demonstrated only one positive HCG level in 40 women studied over a 3-month period. This incidental rate is also similar to women who are not using contraception.

Inhibition of ovulation is the primary mechanism of action of oral contraceptive pills. Secondary actions are changes in the endometrium that can prevent implantation, and changes in the cervical mucous that interfere with sperm motility. Oral contraceptives do not have an effect on an established pregnancy.⁴ There is also no evidence that postcoital (emergency) contraception can interrupt an established pregnancy.⁵ Clinicians may choose to include this reassuring data when counseling patients on contraception.

Heathher Paladine, MD
Portland, Ore

References

1. Klaus H, Goebel J, Woods RE, Castles M, Zimny G. Use-effectiveness and analysis of satisfaction levels with the Billings Ovulation Method: two-year pilot study. Fertil Steril. 1977;28(10):1038-1043.
2. Segal SJ, Alvarez-Sanchez F, Adejuwon CA, Brache de Mejia V, Leon P, Faundes A. Absence of chorionic gonadotropin in sera of women who use intrauterine devices. Fertil Steril. 1985;44(2):214-218.
3. Wilcox AJ, Weinberg CR, Armstrong EG, et al. Urinary human chorionic gonadotropin among intrauterine device users: detection with a highly specific and sensitive assay. Fertil Steril. 1987;47:265-269.
4. Guillebaud J. Contraception, Your Questions Answered. New York, NY: Churchill Livingstone, an imprint of Harcourt Publishers Limited; 1999.
5. Glasier A. Drug Therapy: Emergency Postcoital Contraception. N Engl J Med. 1997;337:1058-1064.

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