Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ovulation Induction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources
PubMed1987

Induction of ovulation in polycystic ovary syndrome with a combination of a luteinizing hormone-releasing hormone analog and exogenous gonadotropins.

Eight clomiphene citrate (150 mg/day for 5 days)-resistant anovulatory women with polycystic ovary were included in this study. A luteinizing hormone-releasing hormone (LH-RH) analog, D-Trp-6-LH-RH, 100 micrograms subcutaneous-per day, induced a hypogonadotropic state within varying periods but at most within 3 weeks, after an initial flare-up effect characterized by slight increase in ovarian size in four patients and in the other four by cysts that disappeared rapidly. On the 28th day or 15 to 20 days after menstruation for subsequent cycles, during maintenance of D-Trp-6-LH-RH therapy, a usual gonadotropin regimen was carried out in 33 cycles. Human menopausal gonadotropins obtained follicular maturation in all cycles. However, there was never the growth of a single dominant follicle but always of several follicles. Human chorionic gonadotropin then induced ovulation in 31 cycles (94%). Luteal phase was normal in 28 and inadequate in 3 of the 31 ovulatory cycles. Hyperstimulation, generally mild to moderate but rather severe in 2 cycles, was constant. Five pregnancies were obtained. The overall pregnancy rate was 15% per cycle and 17.8% per normoovulatory cycle. This study showed that an associated treatment with an LH-RH analog enables gonadotropins to achieve ovulation regularly with an encouraging number of pregnancies but at a risk of hyperstimulation.

Adult↗
PubMed1989

Induction of ovulation with clomiphene citrate in women with polycystic ovary syndrome: the difference between responders and nonresponders.

To identify why some women with polycystic ovary syndrome (PCO) fail to respond to clomiphene citrate (CC), the authors have monitored the endocrine and ovarian response to CC 100 mg/day given for 5 days. Of 40 cycles studied in 27 women, 73% were ovulatory. In 8 of 9 anovulatory women, there was no follicular development despite a significant rise in serum gonadotrophin concentrations within 3 to 5 days of starting CC. There were no significant differences between the ovulatory and anovulatory groups in the peak response of either luteinizing hormone (LH) or follicle-stimulating hormone (FSH). The authors conclude that, in women with polycystic ovaries, the most common reason for the failure to ovulate is an absent ovarian response to an appropriate rise in serum FSH.

Adult↗
PubMed1989

Induction of ovulation with subcutaneous pulsatile gonadotropin-releasing hormone: correlation with body weight and other parameters.

We treated 21 anovulatory infertile patients with subcutaneous pulsatile gonadotropin-releasing hormone (GnRH) administered via a syringe pump. Response to treatment was assessed by urinary estrogen excretion and ultrasound measurement of follicular growth. Ten patients ovulated and 8 subsequently conceived, for a total of 10 pregnancies. Human chorionic gonadotropin (hCG) was not administered routinely, but two patients required hCG to induce follicular rupture. The majority of the patients who conceived had a body mass index (BMI) of less than 21 and a luteinizing hormone (LH)/follicle-stimulating hormone ratio of less than 1. Conversely, those patients with either elevated BMI or LH or both generally failed to respond satisfactorily to this treatment. It is suggested that pulsatile GnRH is most likely to succeed in inducing ovulation if the BMI is less than 21 and the LH is normal, but is unlikely to be successful if there is both an elevated LH and a BMI of greater than 25. Between these two extremes, the response is variable and a therapeutic trial may be appropriate.

Anovulation↗
PubMed1999

Induction of ovulation with the use of a starting dose of 50 units of recombinant human follicle-stimulating hormone (Puregon).

OBJECTIVE: To determine whether a starting dose of 50 units of recombinant FSH (follitropin beta, Puregon; Organon Laboratories Limited, Cambridge, United Kingdom) produces a follicular response in patients with clomiphene citrate-resistant polycystic ovary syndrome (PCOS). DESIGN: Prospective observational study. SETTING: Routine clinical practice in a teaching hospital fertility unit. PATIENT(S): Patients with clomiphene citrate-resistant PCOS who wanted to become pregnant. INTERVENTION(S): Low-dose step-up protocol of SC recombinant FSH administration, monitored prospectively by transvaginal ultrasonography and retrospectively by serum endocrine assays taken at each monitoring visit. MAIN OUTCOME MEASURE(S): Rate and size of follicular growth, recombinant FSH requirement, E2 response, ovulation, cycle cancellation, and pregnancy. RESULT(S): All patients exhibited a follicular response: Six patients ovulated, of whom two conceived and four had their cycles cancelled because of overstimulation. One patient did not ovulate despite the development of a follicle. CONCLUSION(S): Recombinant FSH can be used successfully to stimulate follicular growth at a starting dose of 50 IU.

Adult↗
PubMed2004

Induction of ovulation in nonlactating dairy cows and heifers using different doses of a deslorelin implant.

The objective of this study was to evaluate ovarian function after inducing ovulation with a deslorelin implant in nonlactating dairy cows and heifers. Cattle received GnRH on Day -9, and PGF2alpha on Day -2. On Day 0, in Experiment 1, cows received either 100 microg GnRH (Control), a 750 microg (DESLORELIN 750) or 1000 microg (DESLORELIN 1000) deslorelin implant. On Day 0, in Experiment 2, cows received 100 microg of GnRH or a 450 microg (DESLORELIN 450) deslorelin implant. In Experiments 1 and 2, cows received PGF2alpha on Day 16. Ultrasonography and blood sampling for plasma progesterone (P4) were used to monitor ovarian activity. On Day 0, in Experiment 3, heifers received either 100 microg of GnRH or 750 microg (DESLORELIN 750) deslorelin implant. On Day 16, all heifers received PGF2alpha. Blood samples were collected on Days 7, 13 and 16. In Experiments 1-3, deslorelin implants did not elevate plasma concentrations of P4 in a systematic manner during the late luteal phase. In Experiments 1 and 2, deslorelin implants decreased the size of the largest follicle and the number of Class II and III follicles. In Experiments 1 and 2, deslorelin-treated cows failed to ovulate by Day 28. In conclusion, deslorelin implants induced ovulation, stimulated development of a normal CL, and delayed follicular growth during the subsequent diestrus period. For future applications, the dose of the deslorelin implant will have to be adjusted, and if used for timed-inseminations, nonpregnant cows will have to be resynchronized to minimize delayed returns to estrus and ovulation.

Animals↗
PubMed1998

Ovarian follicular wave synchronization and induction of ovulation in postpartum beef cows.

An experiment was designed to evaluate a) the effect of a progesterone-estradiol combined treatment on ovarian follicular dynamics in postpartum beef cows, and b) ovulation and the subsequent luteal activity after short-term calf removal and GnRH agonist treatment. Multiparous Angus cows (25 to 40 d after calving) were assigned to the following treatments: untreated (Control, n = 9); short term calf removal (CR, n = 8); progesterone (CIDR, n = 9) and progesterone plus estradiol-17 beta (CIDR + E-17 beta, n = 9). Progesterone treatment (CIDR) lasted 8 d and the day of device insertion was considered as Day 0. Cows in the CIDR + E-17 beta group also received an i.m. injection of 5 mg of E-17 beta on Day 1. On Day 8, calves were removed for 48 h (CR, CIDR and CIDR + E-17 beta groups) and 6 h before the end of calf removal these cows also received an i.m. injection of 8 micrograms of Busereline (GnRH). Anestrus was confirmed in all cows by the absence of luteal tissue and progesterone concentrations below 1 ng ml-1 at the beginning of the experiment. Although mean (+/- SEM) interval from the beginning of the experiment (Day 0) to wave emergence did not differ (P > 0.05) among treatment groups (Control, 1.9 +/- 1.0, range -2 to 7 d; CR, 3.9 +/- 0.7, range 0 to 6 d; CIDR, 2.8 +/- 0.5, range 0 to 4 d and CIDR + E-17 beta, 4.1 +/- 0.2, range 3 to 5), the variability was less (P < 0.05) in the CIDR + E-17 beta group. The proportion of cows ovulating 24 to 48 h after GnRH administration tended (P = 0.08) to be higher in cows from CIDR + E-17 beta group (8/9) than in those of CR (5/8) or CIDR (6/9) groups, respectively and was associated with a higher proportion (P < 0.05) of CIDR + E-17 beta treated cows (9/9) that had a dominant follicle in the growing/early static phase at the time of GnRH treatment compared to the other GnRH treated groups (5/8, and 4/9 for CR and CIDR groups, respectively). Two CR cows ovulated 0-24 h after GnRH and only one Control cow ovulated the day before the time of GnRH administration. Cows pretreated with progesterone had longer (P < 0.05) luteal lifespan (CIDR, 14.5 +/- 0.7, CIDR + E-17 beta, 13.9 +/- 0.6 d) than those not treated with CIDR (Control, 5, CR, 4.0 +/- 0.4). We conclude that progesterone plus estradiol treatment results in tightly synchronized wave emergence and high GnRH-induced ovulation rate with normal luteal activity in postpartum beef cattle.

Administration, Intravaginal↗
PubMed1999

Modification of follicular dynamics by exogenous FSH and progesterone, and the induction of ovulation using hCG in postpartum beef cows.

Follicular growth and ovulation in response to FSH, progesterone and hCG were evaluated in postpartum beef cows. In Experiment 1, on Day 21 post partum, cows received an injection of either saline (control; n = 6), FSH (200 mg; n = 6), or a PRID (n = 5) for 10 d. Both FSH and PRID prolonged maintenance of a dominant follicle (15.5 +/- 1.16 and 14.4 +/- 1.29 d, respectively, vs 8.4 +/- 1.22 d in control; P < 0.01), and increased the maximum diameter of the dominant follicle (14.0 +/- 0.91 and 16.4 +/- 1.01 mm, respectively, vs 10.9 +/- 0.95 mm in control; P < 0.05). The PRID-maintained dominant follicle ovulated in 60% of cows, followed by normal estrous cycles (vs 0% in control; P = 0.01), whereas the dominant follicle ovulated in 33% of FSH-treated cows (P = 0.08). The PRID regimen shortened the interval to first ovulation preceding a normal cycle and continued cyclicity (44 +/- 4.1 vs 60 +/- 4.4 d in control; P = 0.02). In Experiment 2, on Day 21 post partum, cows received either saline (control), saline + PRID, or FSH + PRID (n = 16/group). Sixty hours after PRID withdrawal, cows received either saline or hCG (1,500 IU, n = 8/treatment). The FSH + PRID regimen increased the number of large (> 10 mm in diameter) follicles (3.6 +/- 0.43 vs 1.9 +/- 0.39 in control; P = 0.005). Both PRID and FSH + PRID prolonged maintenance of the largest follicle (11.0 +/- 0.82 and 11.2 +/- 0.91 d, respectively, vs 8.7 +/- 0.81 d in control; P < 0.05). The PRID-maintained dominant follicle ovulated in 50% of cows, followed by normal estrous cycles. The FSH + PRID-maintained largest follicle had become atretic at PRID withdrawal and was anovulatory. The FSH + PRID + hCG regimen increased the incidence of ovulation preceding a cycle of normal duration and continued cyclicity (100 vs 50% in PRID; P = 0.03), and reduced the interval to first ovulation preceding a cycle of normal duration and continued cyclicity (38 +/- 6.5 vs 58 +/- 6.3 d in control; P = 0.04). The area under the progesterone curve during the induced cycle was reduced after (PRID +/- FSH) + hCG than after PRID +/- FSH (P = 0.002). These results indicate that PRID alone or with FSH/hCG has the potential to modify the dominant follicle and initiate cyclicity in postpartum beef cows.

Animals↗
PubMed2003

Apoptosis in human granulosa cells after induction of ovulation in women participating in an intracytoplasmic sperm injection program.

OBJECTIVES: To investigate whether analysis of granulosa cell apoptosis can be useful in assessing follicular and oocyte maturation and the regulation of granulosa cell apoptosis by follicular fluid steroids in preovulatory follicles of stimulated women. STUDY DESIGN: Apoptosis in aspirated granulosa cells (n=64) was measured using the Annexin V-affinity assay by flow cytometry. Follicular fluid steroids were determined by ELISA and RIA. Statistics were evaluated using the Levenne test, Student t-test and simple linear regression analysis. RESULTS: No significant differences in the number and percentage of apoptotic granulosa cells per follicle were observed according to the maturity and fertilizability of the oocytes by intracytoplasmic sperm injection within these follicles. No correlations were found between levels of steroid hormones in follicular fluid and the number and proportion of granulosa cells undergoing apoptosis. CONCLUSIONS: The percentage of apoptosis in granulosa cells is not related to oocyte maturity and fertilizability by ICSI or to follicular quality in stimulated cycles of normal women. However, the possibility cannot be discarded that this parameter may be of importance at other phases of follicular development or in natural cycles when no treatment that influences follicular physiology is being applied.

Annexin A5↗
PubMed1990

Induction of ovulation for assisted reproduction programmes.

The decision to use enhancement of the natural ovarian/menstrual cycle to attempt collection of several oocytes during IVF and GIFT cycles has dramatically increased the pregnancy rates. Furthermore, the recovery of multiple fertilizable oocytes allows for cryopreservation of extra or surplus pre-embryos (or embryos), with the consequent reduction in the risk of multiple pregnancies and the improvement of the cumulative pregnancy rate following IVF and GIFT cycles. Here, we have reviewed the underlying physiological mechanisms in the natural ovarian-menstrual cycle. Subsequently, we have analysed the more frequently utilized ovarian stimulatory regimens with special emphasis on the use of gonadotrophins. Several conclusions may be drawn from the experience to date with these methods of ovarian stimulation. Primarily, lower doses of medication, when used appropriately, may result in a more favourable outcome. Most significant, it seems to be beneficial to tailor the dosages and timing of drug administration to the patient's individual response to medication. Because ovarian stimulation therapy is difficult to manage, a major challenge in reproductive endocrinology has been to develop stimulation protocols that would 'ideally' synchronize the development of a cohort of follicles. The development of GnRH analogues (agonists and antagonists) and the experience (both in women and macaques) gained so far when these drugs are used in combination with gonadotrophins, have helped both in the understanding of the underlying physiology and in the improvement of clinical results.

Female↗
PubMed1990

Induction of ovulation with pulsatile GnRH.

The use of pulsatile GnRH to treat infertile women who do not ovulate has been shown to be safe, simple, and effective and the preferred method of inducing ovulation in appropriately selected patients who are resistant to treatment with clomiphene citrate. Treatment with GnRH is particularly effective for restoring ovulation in patients with idiopathic hypogonadotrophic hypogonadism and partially recovered weight-related amenorrhoea, but less successful in patients with polycystic ovary syndrome and organic hypothalamic pituitary disease. Based on personal experience, we advocate routine use of the subcutaneous route, using 15 micrograms per pulse every 90 min, and we monitor the patient's progress by serial ultrasound scanning and measurement of serum gonadotrophin and oestradiol concentrations. If the patient does not respond we recommend adding treatment with clomiphene citrate (Homburg et al, 1988b). Treatment with intravenous GnRH is reserved for women who do not respond to the above combination of drugs. We do not treat patients with GnRH until their body mass index is in the normal range (between 20-25) and we avoid GnRH treatment in patients with hypersecretion of LH during the follicular phase. If LH concentrations are raised, an alternative method of treatment is recommended, such as ovarian diathermy (Armar et al, 1990). Finally, the question of whether GnRH deficiency in patients with hypogonadotrophic hypogonadism is caused by a specific genetic lesion is not yet fully resolved. Yang-Feng et al (1986) used a cDNA clone encoding the human GnRH precursor molecule in order to assign the GnRH gene to a particular human chromosome. They found a single site for GnRH sequences in the human genome and that the gene coding for GnRH is located on the short arm of chromosome 8. Experiments in the congenitally hypogonadal mouse have shown that it is possible to restore gonadal development and gametogenesis by gene transfer (Mason et al, 1987). Clearly an abnormality at the level of the genome may be responsible for the secretory defect in patients with hypogonadotrophic hypogonadism, but it has yet to be defined (Weiss et al, 1989). Presumably elucidation awaits the development of more refined methods because both the genetics and the clinical associations of GnRH deficiency are most persuasive. Meanwhile replacement treatment with GnRH provides a simple and safe form of treatment for managing the clinical syndromes of GnRH deficiency.

Anovulation↗
PubMed1990

Common problems in induction of ovulation.

There are many groups of women with anovulatory infertility who respond abnormally to conventional treatment. It is important to diagnose the underlying disorder correctly before commencing treatment. In this chapter we have discussed the various treatment modalities available and how they may be adapted to fit the particular clinical needs. In women who are profoundly hypo-oestrogenic, the 'priming' of the ovary using prolonged low-dose gonadotrophins offers a possible solution if both subcutaneous and intravenous pulsatile GnRH therapy has failed. It may also reduce the incidence of multiple pregnancies in these women. Growth hormone seems to augment the response to gonadotrophin in these women and may prove a useful adjunct to therapy once further experience of its use has been reported. Women with PCO have been a difficult group to treat because of their tendency to hyperstimulate. The low-dose gonadotrophin regimen outlined in this chapter overcomes the majority of these problems without reducing the rate of conception. This group continue to have an increased incidence of miscarriage. The introduction of combined therapy of hMG with a GnRH analogue may improve this situation, but the data from randomized controlled studies are still awaited. Ovarian failure remains an untreatable cause of infertility. A few women may become pregnant spontaneously, but these are the exception rather than the rule. Hormone replacement therapy should be offered to all these women because of the long-term problems of osteoporosis and cardiovascular disease. Products containing a low dose of oestrogen (e.g. Premarin 0.625 mg) will not interfere with ovulation if there should be a spontaneous resumption of ovarian activity.

Anovulation↗
PubMed2006

Safety of IVF under anticoagulant therapy in patients at risk for thrombo-embolic events.

The objective of this study was to assess the safety of induction of ovulation and oocyte retrieval in patients at risk of thrombosis, necessitating treatment with anticoagulants. Twenty-four patients considered as high risk for a thromboembolic event underwent 73 IVF cycles and 68 oocyte retrieval procedures, and were treated concomitantly with anticoagulation therapy (low molecular weight heparin; LMWH). A subgroup of five patients considered at especially high risk for thrombosis was isolated. These patients were prepared for oocyte retrieval using a controlled spontaneous cycle. All these patients were programmed exclusively for surrogacy. Nineteen women underwent 49 cycles of ovulation induction with gonadotrophins. The average peak oestradiol concentration was 1791 +/- 1420 pg/ml with an average of 13.5 +/- 8.4 oocytes retrieved in each cycle. The five patients from the very high risk group underwent 24 cycles: the average peak oestradiol concentration was 163 +/- 98 pg/ml. In 18, an egg was retrieved and in 14, fertilization was achieved. No bleeding or thromboembolic complications were noted during treatment of both groups of patients. It is concluded that during induction of ovulation in patients at risk for thrombosis, the introduction of LMWH as a cycle protective treatment was not associated with any medical complication. The use of a controlled spontaneous cycle with LMWH is suggested in very high risk patients.

Adult↗
PubMed1984

Induction of ovulation and fertility in amenorrheic women by pulsatile low-dose gonadotropin-releasing hormone.

In functional hypothalamic amenorrhea, failure of ovulation probably results from deficient hypothalamic secretion of gonadotropin-releasing hormone (GnRH). We treated 14 infertile women in whom this condition was resistant to clomiphene with pulses of 5 to 15 micrograms of GnRH administered subcutaneously by portable pumps at 90-minute intervals in 36 cycles of treatment. Ovulation occurred in 30 cycles (83 per cent) and was followed by normal luteal function in 24. Singleton pregnancy occurred after 13 (54 per cent) of these cycles. Ovarian ultrasound consistently showed a single dominant follicle, and follicular-phase levels of gonadotropins and urinary estrone glucuronide were in the normal range in all cycles of treatment except two in which mild ovarian overstimulation occurred. Plasma profiles of GnRH and luteinizing hormone were highly pulsatile after subcutaneous administration of GnRH, and mean peak plasma levels of GnRH were comparable to those in pituitary portal blood. We conclude that treatment with low-dose subcutaneous pulses of GnRH is a safe, effective, and physiologic method of restoring reproductive function in hypothalamic amenorrhea and that it has advantages over gonadotropin therapy.

Adult↗
PubMed2000

Induction of ovulation in infertile women with hyperandrogenism and insulin resistance.

The polycystic ovary syndrome is a common cause of anovulatory infertility. Women with severe insulin resistance are a unique subset of polycystic ovary syndrome. The syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN syndrome) is one presentation of the insulin-resistant subset of polycystic ovary syndrome. Insulin resistance and hyperandrogenism are caused by genetic and environmental factors. In women with anovulatory infertility caused by hyperandrogenism and insulin resistance, clomiphene citrate treatment often fails to result in pregnancy. For these women, weight loss and insulin sensitizers can be effective methods of inducing ovulation and pregnancy and may reduce the number of clomiphene-resistant women with polycystic ovary syndrome who are treated with gonadotropins, ovarian surgery, or in vitro fertilization-embryo transfer.

Acanthosis Nigricans↗
PubMed1994

Ovulatory activity, hormonal induction of ovulation and fertility of young Cashmere and Angora female goats in a temperate environment.

Reproductive parameters of young Cashmere and Angora goats born between 1988 and 1990 and grazed on temperate pastures in southern Australia were examined with a view to reducing the age of first breeding. Females born in August or October of 1989 and 1990 were examined each month by laparoscopy to determine natural ovulatory activity when 6-19-months old. Cashmeres commenced ovulating as young as 7 months of age or as light as 12 kg. Almost all Cashmeres were ovulating by 8-10 months of age at a liveweight of at least 18 kg, and their breeding season extended from April to October. By comparison with Cashmeres, Angoras grew more slowly, fewer ovulated, they commenced ovulation later, their ovulation rates were lower and their breeding season was shorter. A stratified sample of these females was injected with 200 I.U. or 400 I.U. of pregnant mare serum gonadotrophin (PMSG) after treatment with controlled internal drug release (CIDR) devices for 16-18 days to induce ovulation at 6, 9, 12, 15 and 19 months of age. Ovulation rates after CIDR-PMSG treatment were higher for Cashmeres than for Angoras and tended to be higher for females injected with 400 I.U. PMSG than 200 I.U. PMSG. The proportion of females remaining anovulatory after exogenous hormonal treatment was higher for Angoras than for Cashmeres (38% and 10% respectively) but it was not affected by the dose of PMSG or age. For kids born in 1989, the kidding rates to insemination (with follow-up mating) after CIDR-PMSG treatment for 8-month-old and 20-month-old Cashmeres (in the breeding season) were similar (75.0% and 83.8% respectively) but the rate for 14-month-old Cashmeres was only 10.0% (in the non-breeding period). The kidding rates for Angoras bred at 8, 14 and 20 months of age were 8.4%, 20.0% and 30.0% respectively. Ovulatory activity and fertility in the non-breeding period, with or without CIDR-PMSG treatment, did not improve with melatonin treatment.

Animals↗
PubMed2002

Surgical induction of ovulation in polycystic ovarian disease.

The current lines of treatment of an ovulatory infertility due to polycystic ovarian disease lie between weight loss, insulin sensitising agents, clomiphene citrate, gonadotrophin therapy, or finally ovarian cauterisation. This review is looking at some of the current evidence for surgical and medical lines of treatment.

Anovulation↗