Future use of clomiphene in ovarian stimulation. Will clomiphene persist in the 21st century?

Tarlatzis, Basil C.; Grimbizis, G

doi:10.1093/humrep/13.9.2356

Cited by 25 publications

(7 citation statements)

References 53 publications

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“…In the largest cohort study published to date, Kurachi and colleagues reported a 2.2% malformation rate in 935 infants born following clomiphene-induced ovulation versus a 1.7% rate in 30 033 infants born after spontaneous ovulation, a non-significant difference 6 . The overall clinical experience indicates that the use of clomiphene is associated with an incidence of birth defects similar to that observed in the general population 12 .…”

Section: Discussionsupporting

confidence: 53%

Pregnancy outcomes with increased clomiphene citrate dose

Jain

Kuo

2004

Gynecological Endocrinology

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Our objective was to evaluate whether ovulation induction with an increased clomiphene citrate dose of 150-250 mg/day for 5 days adversely affected pregnancy outcome. A retrospective chart review of 1910 medical records yielded 119 pregnancies with sufficient information regarding domiphene dose and pregnancy outcome. Of the 84 pregnancies that followed clomiphene doses of 50-100 mg/day, 32.1% ended in spontaneous abortion, 10.7% in ectopic gestation, 1.2% with congenital malformations, 2.4% in stillbirth and 53.6% in normal gestation. Of the 35 pregnancies that followed clomiphene doses of 150-250 mg/day, 34.3% ended in spontaneous abortion, 5.7% in ectopic gestation, 2.9% with congenital malformations, 2.9% in stillbirth and 54.3% in normal gestation. These differences were not statistically significant. These data suggest that a clomiphene dose of 150-250 mg/day does not appear to increase adverse pregnancy outcomes.

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Section: Discussionsupporting

confidence: 53%

Pregnancy outcomes with increased clomiphene citrate dose

Jain

Kuo

2004

Gynecological Endocrinology

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“…It is well known that the addition of gonadotropins in CC cycles is accompanied by a more intense ovarian response than the use of CC alone. In addition, there is a lower need for gonadotropins as compared to the GnRH agonist/gonadotropin regimes as well as an improved endometrial pattern and receptivity [29]. Having failed 6 cycles of CC therapy, it is possible that CC alone is unable to generate an optimum amount of endogenous gonadotropin (FSH) necessary for the development of competent follicles and inducing ovulation.…”

Section: Discussionmentioning

confidence: 99%

Comparison of letrozole with continuous gonadotropins and clomiphene-gonadotropin combination for ovulation induction in 1387 PCOS women after clomiphene citrate failure: a randomized prospective clinical trial

Ganesh

Goswami

Chattopadhyay

et al. 2009

J Assist Reprod Genet

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Purpose Letrozole, though reported to be an effective ovulation inducing agent, warrants larger randomized trials. The purpose of this study is to compare the efficacy of letrozole with that of rFSH and clomiphene citrate(CC)/rFSH for ovarian stimulation in IUI cycles. Methods Randomized, prospective, single-blinded clinical trial. 1387 PCOS women after CC failure were randomized into three groups: Group A received letrozole, Group B received CC with two doses rFSH and Group C received continuous rFSH day 2 onwards until hCG injection. Results Group A, B and C had an ovulation rate of 79.30%, 56.95% and 89.89% and cycle cancellation rate of 20.70%, 43.05% and 10.11%, respectively. Pregnancy rates in Group A, B and C were 23.39%, 14.35% and 17.92%, while the miscarriage rates were 13.80%, 16.67% and 14.52%, respectively. Conclusion Letrozole appears to be a suitable ovulation inducing agent in PCOS women with CC failure and is found to be most effective when baseline estradiol level >60 pg/ml.

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“…In terms of isoform specificity, clomifene has been shown to agonize and antagonize ERa but only antagonize ERb (Kurosawa et al, 2010). The mechanism of action ascribed to clomifene in infertility treatment involves antagonism in the hypothalamus, which increases levels of gonadotropin-releasing hormone (GnRH) and subsequently increases folliclestimulating hormone (FSH) and luteinizing hormone (LH) secretion (Dickey and Holtkamp, 1996;Tarlatzis and Grimbizis, 1998). It has also been suggested that clomifene may inhibit the estradiol-dependent proliferation of endometrial epithelial cells by inhibiting the recruitment of SRC1 to ERa and thus estradioldependent ER transactivation (Amita et al, 2010).…”

Section: Nuclear Receptors and Their Selective Modulatorsmentioning

confidence: 99%