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REVIEW ARTICLE
Year : 2014  |  Volume : 1  |  Issue : 1  |  Page : 6-11

Use of oral contraceptives in assisted reproductive cycles


InVia Fertility Specialists, SC, Hoffman Estates, IL, USA

Date of Web Publication14-Feb-2014

Correspondence Address:
Vishvanath Chandrakant Karande
InVia Fertility Specialists, SC, Hoffman Estates, IL
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2348-2907.127082

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  Abstract 

Oral contraceptive (OC) pills are commonly used in patients undergoing in vitro fertilization to schedule cycle starts. This often helps with staff scheduling and efficiency. In this paper, the use of OC pre-treatment in assisted reproductive cycles will be discussed. The focus will be on the use of OC in gonadotropin releasing hormone (GnRH) antagonist cycles, GnRH agonist cycles, poor responders and finally in high responders. A recent meta-analysis of six randomized control trials concluded that in cycles with GnRH-antagonist protocols, OC pre-treatment: (1) Increases the duration of stimulation, (2) increases the total dose of gonadotropins and (3) resulted in a small but significant reduction in pregnancy rates. All these studies used pure follicle stimulating hormone for controlled ovarian hyperstimulation. These conclusions, however, may not be valid in cycles where the birth control pill free interval is 5 days, and there is use of combination protocols (luteinizing hormone or human menopausal gonadotropin add back). 17β-estradiol (E2, 4 mg/d) pre-treatment is a viable alternative to using OC. However, in these patients, gonadotropin stimulation should be started on the first day of estrogen discontinuation. In GnRH agonist cycles, pre-treatment with OC reduces the formation of functional ovarian cysts and may reduce the incidence of ovarian hyperstimulation syndrome.

Keywords: Birth control pills, gonadotropin releasing hormone agonists, gonadotropin releasing hormone antagonists, oral contraceptives


How to cite this article:
Karande VC. Use of oral contraceptives in assisted reproductive cycles. IVF Lite 2014;1:6-11

How to cite this URL:
Karande VC. Use of oral contraceptives in assisted reproductive cycles. IVF Lite [serial online] 2014 [cited 2022 Jan 18];1:6-11. Available from: http://www.ivflite.org/text.asp?2014/1/1/6/127082


  Introduction Top


For several years now, research has focused on making in vitro fertilization (IVF) cycles more efficient and convenient. [1],[2] Scheduling of cycles is common practice in order to avoid weekend retrievals and equally distribute the workload throughout the week. A planned distribution of the workload avoids excessive incubator door openings and their negative impact on embryo development. It also helps with better work schedules for embryology and nursing staff and avoids unplanned work that may result in loss of concentration and reduced efficiency.

There are several ways with which cycle scheduling can be done: (1) a flexible start of the stimulation because results do not seem to change whether ovarian stimulation is started on day 2 or day 3 of the cycle; [3] (2) delaying or advancing human chorionic gonadotropin administration, because moving it 1 day ahead or postponing one extra day does not seem to influence cycle outcome; [4] (3) estradiol (E2) pre-treatment in the late luteal phase to avoid follicle stimulating hormone (FSH) rise and follicle recruitment [5],[6] and (4) pre-treatment with oral contraceptive (OC) pills. [7]

The use of OC pre-treatment for cycle scheduling is fairly common. The estrogen component will avoid FSH rise and follicle recruitment and progesterone (P) will avoid luteinizing hormone (LH) rise. However, recently, there has been a controversy about the negative impact of their use on IVF success rates. [8],[9] This controversy and other issues regarding the use of OC pre-treatment in various stimulation protocols will now be discussed in detail.


  Use of OC In Gonadotropin Releasing Hormone Antagonist Cycles Top


In the long gonadotropin releasing hormone (GnRH) agonist protocol, ovarian stimulation is initiated once pituitary desensitization has been achieved. Cycle starts can be postponed for a few days just by continuing the agonist. The initiation of stimulation in GnRH antagonist protocols however relies on the occurrence of menstruation. These protocols therefore do not allow for programming of IVF cycles unless there is pre-treatment of some sort. The use of GnRH antagonists may be associated with a slight reduction in number of retrieved oocytes. This has been partly attributed to the absence of synchronization of the follicular cohort before ovarian stimulation. [10] Pre-treatment with OC was an obvious solution to both these potential problems and their use is now widespread. Stimulation protocols using GnRH antagonists have the advantage of being shorter, utilize fewer injections and have a lower incidence of ovarian hyperstimulation syndrome (OHSS) when compared to protocols using GnRH agonists. This results in IVF cycles becoming more "patient friendly" with lower dropout rates. [11]

A variety of OC have been used for pre-treatment in ART cycles. The dose of ethinyl E2 in OC can vary from 15 to 50 μg. The type of progestogen used also varies and includes norethindrone, norgestimate, desogestrel or levonorgestrel.

The publications so far have been limited to the use of monophasic OC. The use of triphasic OC in GnRH antagonist cycles has not been evaluated.

The pill-free interval also varies with a period of 2-5 days being reported in the literature. [8] A 5-day wash-out period after OC was shown to be optimal prior to initiation of gonadotropins. Cédrin-Durnerin et al. prospectively assessed hormonal and ultrasound data collected during the free period after the discontinuation of three different pre-treatments to provide information on the optimal time interval required before starting stimulation. [12] Women were randomized to receive OC (ethinyl E2 30 μg + desogestrel 150 mg) (n = 21) or norethisterone 10 mg/day (n = 23) or 17β E2 4 mg/day (n = 25) or no pre-treatment (n = 24) for one cycle before IVF. Assessments were performed on the post-treatment day (PD) 1, 3 and 5, or on spontaneous cycle day (CD) 1 and 3. They found that after OC and progestogen administration, FSH and LH concentrations shifted from strongly suppressed PD1 levels to PD5 values similar to those observed on CD1. Meanwhile, follicle sizes remained small up to PD5. In contrast, estrogen pre-treatment poorly reduced FSH levels on PD1 compared with OC or progestogen. Consequently, follicle size was more heterogeneous. FSH rebound was maximal on PD3, whereas LH levels were slightly increased up to PD5. They concluded that a 5-day free interval after OCP or progestogen offers the advantages of gonadotropin recovery and homogeneous follicular cohort, whereas early FSH rebound occurring after estrogen pre-treatment argues for a short free period. [12]

The duration of pill administration may also impact control of the cycle and the endometrium. [13] Many publications on this issue have reported the use of OC for 21 days. [8] We have been routinely starting OC on CD 2 or 3 and continuing them for 10-21 days. Use of OC for more than 2 months may result in ovarian suppression and a sub-optimal response to stimulation. [14]

Griesinger et al. initially reported a meta-analysis [15] of four randomized controlled trials (RCTs) encompassing 847 patients. [12],[16],[17],[18] OC pre-treatment was associated with an increased gonadotropin consumption (weighted mean difference [WMD]: +542 IU, 95% confidence interval [CI]: +127-956), an increased duration of stimulation (WMD: +1.41 days, 95% CI: +1.13-1.68) and with a trend toward a reduction in ongoing pregnancy rate (PR) (relative risk [RR] 0.79, 95% CI: 0.60-1.02, P = 0.07).

In an updated meta-analysis, two additional RCTs were included bringing the total of randomized patients to 1,343. The first study was a multinational (United States and Europe) open-label, two-armed RCT in which 442 patients were randomized to either pre-treatment with OC or no OC pre-treatment before ovarian stimulation with 200 IU recombinant FSH in a GnRH antagonist multiple dose protocol. [19] They were between 18 and 39 years of age and had regular menstrual cycle and a body mass index (BMI) ≤32 kg/m 2 . Ovarian stimulation was initiated on day 5 after cessation of the OC or on day 2 or 3 of a spontaneous menstrual cycle. The OC consisted of desogestrel (0.15 mg) and ethinyl E2 (0.03 mg) and was administered for 14-21 days. IVF, intracytoplasmic sperm injection (ICSI), and luteal phase support followed standard practice.

The second study was a single center, three-armed RCT in which a total of 82 low responders (defined as patients with repeated day 3 levels of FSH >8.5 mIU/mL, and/or antral follicle count ≤5) were randomized to ovarian stimulation in one of three different protocols: GnRH antagonist multiple dose protocol after OC pre-treatment, GnRH antagonist multiple dose protocol without OC pre-treatment, or GnRH agonist luteal long protocol without OC pre-treatment. [19] Further inclusion criteria were age 28-41 years and BMI between 19 and 30 kg/m 2 . The OC consisted of ethinyl E2 (0.03 mg) and levonorgestrel (0.15 mg) and were administered for 21 days. Ovarian stimulation with 225 IU recombinant FSH was initiated on day 5 after cessation of the OC or on day 3 of a spontaneous menstrual cycle in the antagonist-treated patients.

All trials used combined OC pills with 30 μg of ethinyl E2 and 150 μg of progestin (either desogestrel or levonorgestrel), and the duration of pill pre-treatment ranged from 14 to 28 days. The pill-free interval between cessation of OC treatment and initiation of stimulation was 2-3 days in two of the studies, [16],[18] whereas in the remaining four studies a 5-day interval was used. Ovarian stimulation was performed with recombinant FSH in all studies. Fertilization methods included both IVF and ICSI, and ETs were performed 2-5 days after oocyte retrieval. Vaginal micronized P was used for luteal phase support in four of the studies, whereas in two multicentric studies [18],[19] luteal phase support was given according to the practice of individual centers.

The probability of an ongoing pregnancy per randomized woman was found to be significantly lower in patients who received OC pre-treatment (RR 0.80, 95% CI: 0.66-0.97; P = 0.02; rate difference: −5%, 95% CI: from −10% to −1%; P = 0.02; odds ratio 0.74, 95% CI: 0.58-0.96; P = 0.02; fixed effects model). There was no statistical significant heterogeneity between individual studies. The exclusion of the study on poor responders [19] increased the effect size (RR 0.78, 95% CI: 0.64-0.94, P = 0.01; rate difference: −6%, 95% CI: −11% to −1%; P = 0.01; fixed effects model).

Duration of stimulation (WMD: +1.33 days, 95% CI: +0.61-2.05; P < 0.01; random effects model) and gonadotropin consumption (WMD: +360 IUs, 95% CI: +158-563; P < 0.01; random effects model) were significantly increased after OC pre-treatment; however, there was statistical significant heterogeneity (P < 0.01) between individual studies for both outcomes. The number of cumulus-oocyte complexes was not significantly different between the groups compared (WMD: +0.6 cumulus-oocyte complexes, 95% CI: −0.08-1.25; P = 0.09; fixed effects model), with no statistical significant heterogeneity between studies.

Thus, the use of OC pre-treatment in antagonist IVF cycles showed a relatively small (−5% rate difference [95% CI: −10% to −1%]) but statistically significant reduction of ongoing pregnancy likelihood with OC pre-treatment when a pill-free interval of 2-5 days is used before starting gonadotropin stimulation. Based on the incidence of ongoing pregnancies in the RCTs included in this meta-analysis, the number-needed-to-treat-to-harm is 20 patients (95% CI: 10-100) (e.g., for every 20 patients pretreated with OC, one ongoing pregnancy will be missed).

The authors could not find a definite reason for this observed reduction in PR with OC pre-treatment. They speculate that the progestin component of the OC could exert a negative impact on endometrial receptivity in the subsequent cycle. Another possibility is that low endogenous LH levels after OC treatment might impair oocyte competence or endometrial receptivity when ovarian stimulation is performed with recombinant FSH void of LH activity in GnRH antagonist cycles, as was the case in all 6 RCTs included in their meta-analysis. It is possible that the addition of LH or use of human menopausal gonadotropin would alter the outcome of OC pretreated GnRH antagonist cycles. They also raised the possibility that use of other progestin/ethinyl E2 combinations may not show this reduction in PR.

Some of the criticisms of this study include the following: The size effect was low; there were many confounding variables (normal as well as low responder patients were mixed, different OC were used with varying days of usage, and varying pill-free interval). [14]

Garcia-Velasco et al. performed a prospective, randomized, controlled trial to assess the effect of OC for cycle scheduling on ongoing PR on women who were normal responders undergoing IVF-ICSI with the antagonist cycle, and compare it with the long-agonist protocol, which is the gold-standard treatment. [14] Regularly cycling women aged <38 years with fewer than three previous IVF attempts were enrolled. Previous low responses to controlled ovarian hyperstimulation (COH), ovarian surgery, or polycystic ovary were exclusion criteria. One hundred fifteen patients received OC (0.030 mg ethinyl E2/0.15 mg desogestrel) for 12-16 days, and COH was started on day 5 after OC treatment; similarly, 113 patients received the long protocol from day 20 to 22 of the previous cycle. Patients receiving the GnRH antagonist treatment showed a lower peak serum E2 (1,334 vs. 1823 pg/mL), lower duration of stimulation (10.3 vs. 11.4 days) with similar FSH consumption (1613 vs. 1807 IU), and ovarian response (10.2 vs. 11.7 oocytes). No differences were observed in the fertilization rates (68.1% vs. 64.8%), total number of embryos obtained (5.9 vs. 6.2), mean number of embryos transferred (1.8 vs. 1.8), implantation rate (36% vs. 39%), miscarriage rate (8.9% vs. 17%), ongoing PR (47.8% vs. 53.9%), or live birth rate (44.3% vs. 47%). They concluded that comparable outcomes could be obtained using OC containing 0.030 mg ethinyl E2/0.15 mg desogestrel to schedule patients undergoing a GnRH antagonist protocol. This study, however, was underpowered, as they needed 377 patients in each group, which was not possible at a single center.

Cédrin-Durnerin et al. [20] assessed the effects of estrogen pre-treatment in GnRH antagonist protocol. This was a prospective randomized multicenter study that analyzed 472 patients undergoing IVF/ICSI. Patients were randomized to receive 17β-E2 (4 mg/d) or no pre-treatment before daily recombinant FSH administration started on 1 st day of estrogen discontinuation or on CD 2 in non-pretreated women. The mean numbers of retrieved oocytes (10.9 + 5.7 vs. 10.2 + 5.6) and obtained embryos (5.5 + 3.7 vs. 4.8 + 3.7) were not significantly different between women allocated to estrogen pre-treatment (n = 238) and no pre-treatment (n = 234). Total FSH amount (1,557 + 408 vs. 1,389 + 347 IU) and stimulation duration (10.8 + 1.4 vs. 10.0 + 1.5 days) were slightly but significantly increased in pretreated patients. Positive pregnancy tests, ultrasound PR, and delivery rate per cycle were similar (36%, 33%, and 26.6%, respectively, vs. 38.2%, 35.4%, and 30%). The authors concluded that estrogen pre-treatment is associated with the requirement of higher FSH doses and longer duration of stimulation without any significant increase in the number of retrieved oocytes. However, estrogen does not affect cycle outcome and therefore might be used in clinical practice for programming IVF retrievals during working days.


  Use of OC In GNRH Agonist Cycles Top


Pituitary suppression with OC prior to initiating GnRH agonist in IVF cycles has been used for many years. [21] The use of OC prior to COH allows for convenient cycle scheduling. In patients treated with the GnRH agonist flare protocol, OC are used for ovulation suppression so that subsequent GnRH agonist treatment cannot stimulate residual corpus luteum function.

OC will also reduce the incidence of functional ovarian cyst formation associated with GnRH agonist use. [22] Biljan et al. postulate that the functional ovarian cysts are probably formed by the transient initial stimulatory effect of GnRH on gonadotropin release. Released gonadotropins in turn cause the rapid growth of primordial follicles. Owing to rapid pituitary suppression, however, continued follicular development and ovulation does not occur and follicular cysts are formed. The initial stimulatory effect of GnRH agonists increases the levels of both FSH and LH. However, early follicular development is caused primarily by FSH, and therefore, the surge of FSH, rather than LH, is probably responsible for functional cyst formation. OC will abolish this initial FSH surge and minimize the risk of formation of functional cysts.

Chung et al. investigated the use of monophasic vs., triphasic OC in GnRH agonist cycles. [23] They found that after ovulation suppression the day 2 FSH and LH values were higher in the group on triphasic OC (4.2 ± 1.8 vs. 6.0 ± 2.6; 2.7 ± 2.0 vs. 4.2 ± 3.3 respectively, P < 0.05). The numbers of oocyte retrieved and fertilization rates were comparable between the two groups, but the triphasic group had higher quality embryos. The implantation and PR were also higher in the triphasic group but were not statistically significant.

Bozdag et al. [24] analyzed the influence of OC pre-treatment in luteal-long leuprolide acetate cycles in normal responder patients (presence of 6-15 antral follicles in both ovaries). They compared the results of 169 study patients with 349 age-matched controls (no OC pre-treatment). The OC group had higher peak E2 levels than the control group (2,630.3 ± 1,568.0 vs. 2,166.5 ± 1,259.7 pg/ml, P = 0.001), higher top quality (>7 blastomeres) embryos on day 3 (4.4 ± 3.3 vs. 3.5 ± 3.1, P = 0.013) and higher embryo transfer cancellation rate (6.5 vs. 2.9%, P = 0.049). The clinical pregnancy (36.7 vs. 38.3%) and implantation rates (21.8 vs. 20.6%) were comparable. They concluded that pre-treatment with OC might exaggerate ovarian response, but does not affect the PR in normal responders.


  Use of OC In Poor Responder Patients Top


Several protocols have been investigated to improve the outcome in this difficult group of patients. [25],[26],[27] In the microdose-lupron (MDL) protocol, [28] patients are usually pre-treated with OC to prevent ovulation and formation of a corpus luteum. It is postulated that the initial stimulation from the MDL could stimulate a residual corpus luteum to premature release of progesterone and resultant luteinization of the uterine lining.

In poor responders using GnRH antagonist protocols, pre-treatment with OC may result in sufficient suppression so as to blunt the subsequent ovarian response. Use of luteal 17β E2 may be a better option in this group of patients. [29],[30] Dragisic et al. have proposed a protocol using a combination of E2 patches and a GnRH antagonist in the luteal phase with encouraging results. [31]


  Use of OC In High Responder Patients Top


Patients with polycystic ovarian syndrome (PCOS) will often show a robust response to gentle stimulation with gonadotropins. They are at an increased risk for OHSS. PCOS patients have higher peak serum E2 levels, lower gonadotropin requirements and will produce a greater number of oocytes than normal responders. They may show a proportionately higher numbers of immature oocytes, lower fertilization rates and poor embryo quality. This may be secondary to the elevated LH levels these patients demonstrate in the follicular phase. GnRH agonists will reduce LH levels in the follicular phase. Pre-treatment with OC prior to starting the GnRH agonist will: (1) permit normalization of the LH/FSH ratio (2) reduce ovarian androgen concentrations and (3) attenuate the initial flare response to the GnRH agonist. Damario et al. [32] have proposed a "dual-suppression" protocol. High-responder patients were started on OC for 25 days followed by s.c. leuprolide acetate 1 mg/d which was overlapped with the final 5 days of OC administration. This approach reduced the cancellation rate and improved the PR with a low incidence of OHSS. Use of the dual method of suppression resulted in significantly lower E2, total testosterone, DHEA-S and androstenedione concentrations at the onset of gonadotropin stimulation in high responders undergoing IVF-embryo transfer. As opposed to GnRH agonist suppression without OC suppression, the dual method of suppression also resulted in significantly lower serum LH. Other groups need to confirm these data in a prospective randomized study. A better option may be to stimulate potential high responder patients with a GnRH antagonist protocol so as to have the option of using a GnRH agonist trigger to minimize the risk of severe OHSS. [33]

 
  References Top

1.Zorn JR, Boyer P, Guichard A. Never on a sunday: Programming for IVF-ET and GIFT. Lancet 1987;1:385-6.  Back to cited text no. 1
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2.Cohen J, Debache C, Solal P, Serkine AM, Achard B, Boujenah A, et al. Results of planned in vitro fertilization programming through the pre-administration of the oestrogen-progesterone combined pill. Hum Reprod 1987;2:7-9.  Back to cited text no. 2
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3.Devroey P, Aboulghar M, Garcia-Velasco J, Griesinger G, Humaidan P, Kolibianakis E, et al. Improving the patient's experience of IVF/ICSI: A proposal for an ovarian stimulation protocol with GnRH antagonist co-treatment. Hum Reprod 2009;24:764-74.  Back to cited text no. 3
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4.Tremellen KP, Lane M. Avoidance of weekend oocyte retrievals during GnRH antagonist treatment by simple advancement or delay of hCG administration does not adversely affect IVF live birth outcomes. Hum Reprod 2010;25:1219-24.  Back to cited text no. 4
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5.le Nestour E, Marraoui J, Lahlou N, Roger M, de Ziegler D, Bouchard P. Role of estradiol in the rise in follicle-stimulating hormone levels during the luteal-follicular transition. J Clin Endocrinol Metab 1993;77:439-42.  Back to cited text no. 5
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8.Griesinger G, Kolibianakis EM, Venetis C, Diedrich K, Tarlatzis B. Oral contraceptive pretreatment significantly reduces ongoing pregnancy likelihood in gonadotropin-releasing hormone antagonist cycles: An updated meta-analysis. Fertil Steril 2010;94:2382-4.  Back to cited text no. 8
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9.Smulders B, van Oirschot SM, Farquhar C, Rombauts L, Kremer JA. Oral contraceptive pill, progestogen or estrogen pre-treatment for ovarian stimulation protocols for women undergoing assisted reproductive techniques. Cochrane Database Syst Rev 2010;1:CD006109.  Back to cited text no. 9
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11.Domar AD, Smith K, Conboy L, Iannone M, Alper M. A prospective investigation into the reasons why insured United States patients drop out of in vitro fertilization treatment. Fertil Steril 2010;94:1457-9.  Back to cited text no. 11
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12.Cédrin-Durnerin I, Bständig B, Parneix I, Bied-Damon V, Avril C, Decanter C, et al. Effects of oral contraceptive, synthetic progestogen or natural estrogen pre-treatments on the hormonal profile and the antral follicle cohort before GnRH antagonist protocol. Hum Reprod 2007;22:109-16.  Back to cited text no. 12
    
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17.Kolibianakis EM, Papanikolaou EG, Camus M, Tournaye H, Van Steirteghem AC, Devroey P. Effect of oral contraceptive pill pretreatment on ongoing pregnancy rates in patients stimulated with GnRH antagonists and recombinant FSH for IVF. A randomized controlled trial. Hum Reprod 2006;21:352-7.  Back to cited text no. 17
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20.Cédrin-Durnerin I, Guivarc'h-Levêque A, Hugues JN. Pretreatment with estrogen does not affect IVF-ICSI cycle outcome compared with no pretreatment in GnRH antagonist protocol: a prospective randomized trial. Fertil Steril. 2012;97:1359-64.e1.  Back to cited text no. 20
    
21.Templeton A, van Look P, Lumsden MA, Angell R, Aitken J, Duncan AW, et al. The recovery of pre-ovulatory oocytes using a fixed schedule of ovulation induction and follicle aspiration. Br J Obstet Gynaecol 1984;91:148-54.  Back to cited text no. 21
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24.Bozdag G, Esinler I, Yaralý H. Pretreatment with oral contraceptive pills does not influence the pregnancy rate in the long leuprolide acetate protocol. Gynecol Obstet Invest 2012;73:53-7.  Back to cited text no. 24
    
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30.Frattarelli JL, Hill MJ, McWilliams GD, Miller KA, Bergh PA, Scott RT Jr. A luteal estradiol protocol for expected poor-responders improves embryo number and quality. Fertil Steril 2008;89:1118-22.  Back to cited text no. 30
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31.Dragisic KG, Davis OK, Fasouliotis SJ, Rosenwaks Z. Use of a luteal estradiol patch and a gonadotropin-releasing hormone antagonist suppression protocol before gonadotropin stimulation for in vitro fertilization in poor responders. Fertil Steril 2005;84:1023-6.  Back to cited text no. 31
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32.Damario MA, Barmat L, Liu HC, Davis OK, Rosenwaks Z. Dual suppression with oral contraceptives and gonadotrophin releasing-hormone agonists improves in vitro fertilization outcome in high responder patients. Hum Reprod 1997;12:2359-65.  Back to cited text no. 32
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33.Griffin D, Benadiva C, Kummer N, Budinetz T, Nulsen J, Engmann L. Dual trigger of oocyte maturation with gonadotropin-releasing hormone agonist and low-dose human chorionic gonadotropin to optimize live birth rates in high responders. Fertil Steril 2012;97:1316-20.  Back to cited text no. 33
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  Authors Top


Dr. Karande is the President, Medical Director, and Director of the IVF Program. After completing his residency in Obstetrics and Gynecology at the State University of New York at Buffalo, NY, he did a Fellowship in the sub-specialty of Reproductive Endocrinology and Infertility at the prestigious Jones Institute for Reproductive Medicine at the Eastern Virginia Medical School in Norfolk, Virginia. Dr. Karande is Board Certified in the specialty of Obstetrics and Gynaecology as well as the subspecialty of Reproductive Endocrinology and Infertility. He is a Fellow of the American College of Obstetricians and Gynecologists and Member of the American Society for Reproductive Medicine.



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