Bulun, S. E. (2003). Ovulation induction in women with infertility: a new indication for aromatase inhibitors. Fertility and Sterility, 80(6), 1338-1339. https://doi.org/10.1016/j.fertnstert.2003.06.001
Bulun SE. Ovulation induction in women with infertility: a new indication for aromatase inhibitors. Fertil Steril. 2003;80(6):1338-1339. doi:10.1016/j.fertnstert.2003.06.001
Bulun, Serdar E. "Ovulation induction in women with infertility: a new indication for aromatase inhibitors." Fertility and Sterility, vol. 80, no. 6, 2003, pp. 1338-1339.
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Aromatase inhibitors promote ovulation, most likely by raising FSH
Aromatase inhibitors promote ovulation, most likely by raising the body's own FSH, a 2003 commentary says. The author reviews one study of women with infertility. Letrozole added to gonadotropin injections appeared to help no more than the injections alone.
Key Findings
Aromatase inhibitors promote ovulation. The most likely mechanism is lower estrogen production in the ovary and other tissues, including the brain, which raises the body's own follicle-stimulating hormone (FSH).
Aromatase inhibitors differ from the estrogen antagonist clomiphene citrate: they exert no direct unfavorable effect on growth and development of the uterine lining during the cycle.
Letrozole added to gonadotropin injections did not seem to benefit a mixed group of women with infertility, compared with gonadotropin-only cycles.
In that comparison, a lower gonadotropin dose was the only apparent gain, and added treatment complexity offset it.
The author suggests that an optimized regimen of gonadotropin plus an aromatase inhibitor may offer an alternative for poor responders to stimulation.
Interpretation
This 2003 commentary reviews one study of women with infertility. Adding letrozole to gonadotropin shots did not add much benefit beyond letting women use a lower gonadotropin dose, and the extra steps offset that gain. The author thinks a tuned mix of gonadotropin plus an aromatase inhibitor may help women who respond poorly to stimulation. He calls for careful, randomized studies of aromatase inhibitors for ovulation induction. He wants the right dose, the right timing, and a clear profile of which women benefit most.
RRM Context
Restorative reproductive medicine evaluates both partners and asks why ovulation is absent or irregular before choosing any agent. The commentary asks for the hormone profiles of women who benefit most, which follows the same cause-based logic. A rise in the body's own FSH, with no direct harm to the uterine lining, fits the restorative principle of working with the cycle. Charting shows whether an ovulatory event follows treatment.
Our editorial summary of this paper, not the article's abstract.
Abstract
The third-generation aromatase inhibitors were initially introduced to treat postmenopausal breast cancer. We now realize that many other potential indications for aromatase inhibitors exist, especially in the field of gynecology. Preliminary data were suggestive that aromatase inhibitors could be used to treat endometriosis and uterine leiomyomata and induce or augment ovulation. Aromatase inhibitors promote ovulation, most likely by increasing endogenous FSH production owing to decreased estrogen biosynthesis in the ovary and extraovarian tissues, including the brain. Aromatase inhibitors differ from the estrogen antagonist clomiphene citrate in that they do not exert a direct unfavorable effect on endometrial growth and development during the menstrual cycle. Healey et al. (1) report important findings on the effects of the addition of an aromatase inhibitor to gonadotropin injections for superovulation. A relatively large number of patients and a control group were studied, and several clinically useful outcomes including pregnancy rates were reported. The addition of letrozole to an ovulation induction regimen using injectable gonadotropins in a mixed population of patients with infertility does not seem to offer any benefits over gonadotropin-only cycles, because the decreased gonadotropin dose (the only apparent benefit) was offset by increased complexity of the treatment. Further randomized clinical trials using a similar design and patient sample may not provide clinically useful data. On the other hand, optimization of this regimen (gonadotropin plus aromatase inhibitor) in poor responders may offer an alternative in this subset of women (2). From the existing literature, it appears that use of an aromatase inhibitor alone to induce or augment ovulation will continue to be an exciting area of research future (3, 4). In particular, the dosing and timing of administration (late luteal versus early follicular) of an aromatase inhibitor for ovulation induction should be optimized. Defining the hormonal profiles of the women who will benefit the most from aromatase inhibition may further increase the success of treatment. In summary, Healey et al. (1) should be congratulated for conducting this interesting work. Carefully designed randomized studies on the use of aromatase inhibitors for ovulation induction or augmentation are warranted.
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