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After ovarian stimulation with clomiphene citrate combined with human menopausal gonadotropin, 24 large (greater than 16 mm) and 16 medium (7 to 15 mm) human follicles were classified according to plasmatic estradiol (E2), luteinizing hormone (LH), and histology of the follicle and oocytes (in thin sections). An asynchronism of several hours between the stage of development of the largest and large cohort follicles is observed; overripeness of oocyte cumulus complex (OCC) is revealed. An asynchronous response to gonadotropins in granulosa and cumulus is also seen in the cohort of medium follicles of the same ovary, but not resumption of nuclear maturation of the oocyte. The efficiency of these oocytes after fertilization is discussed.
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Seven trials (702 participants) were included. There was no significant difference in live birth (55/182 = 30.2 % vs. 47/181 = 26.0 %, p = 0.26, CC + Ant vs. non-CC, respectively), clinical pregnancy (98/346 = 28.3 % vs. 84/356 = 23.6 %, p = 0.12), miscarriage (6/35 = 17.1 % vs. 7/32 = 21.9 %, p = 0.42), endometrial thickness, and on the number of oocytes retrieved. There was a significant reduction in OHSS (1/216 = 0.5 % vs. 9/217 = 4.1 %, p = 0.01), consumption of gonadotropins, and duration of COH.
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All patients received individualized dosing of hMG after 5 days of CC. Transvaginal sonography was performed 15 hours before hCG administration. Intrauterine insemination was performed 36 hours after hCG injection.
Classical ovulation induction produces very good results in normogonadotrophic anovulatory infertility. Alternative treatment options may not be indicated as first-line therapy in these patients, except for subgroups with poor prognosis. These women can be identified by older age, longer duration of infertility and higher insulin:glucose ratio.
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Thirteen patients with clomiphene citrate resistant polycystic ovary syndrome (PCO-CR) were documented by clinical and endocrine profile. Exogenous gonadotropins (HMG, hFSH, hCG), or gonadotrophin releasing hormone agonist (GnRHa) plus gonadotropins represent a new approach to induce ovulation in these (PCO-CR) patients. 92% of these patients ovulated with exogenous gonadotropin, nevertheless the pregnancy rate was only 53%. Five out seven PCO-RC patients did not achieve pregnancy with exogenous gonadotrophins, but they did after ovarian wedge resection. It is interesting to note that four of these patients achieved their second and third pregnancy without any therapy. The authors conclude that the ovarian wedge resection may had to improve in the quality of ovulation in this very selective group of infertile patients.
Mean age was 26.4±3.2 (20-33) and mean BMI was 26.3± 3.2. After treatment using ultrasonography the Resistance index (RI) and Pulsatility index (PI) showed no significant difference among three groups (P > 0.05). Pregnancy rate in letrozole group (58%) was more in comparison to CC (53.6%) and control groups (46%) but the difference was not significant (P > 0.05).
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The present study was designed to investigate the dose-response of clomiphene on several estrogenic responses in the immature rat uterus and to compare it to available data on estradiol-17 beta. A dissociation was demonstrated among the different estrogenic responses induced by clomiphene. Very high doses of clomiphene were needed to induce the 6-h uterine eosinophilia and deep endometrial edema, and maximal response levels were not reached at any dose studied. On the contrary, many genomic responses were induced with much lower doses of clomiphene, and maximal response levels were reached with at least the two highest doses of clomiphene. This dissociation is in agreement with the existence of separate groups of responses that are mediated by multiple and independent mechanisms of estrogen action involving different kind of receptors. Luminal epithelial, glandular epithelial, and myometrial hypertrophies were also found to differ with regard to the dose needed to induce this response in each cell type. The dissociation between genomic responses of the different uterine cell types supports the hypothesis of different estrogen receptors for each kind of cell. Clomiphene induces mitoses in the different cell types, but the proportion of mitoses in the cell types was different from that described for estradiol. It is suggested that these differences are also due to differences between receptors involved in cell proliferation.
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Case report from a randomized clinical trial.
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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.
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After exclusion of primary ovarian failure and causes of infertility not due to contraception, 48 patients with (PPA) post-pill amenorrhea and 47 patients whose amenorrhea did not follow oral contraception received treatment aimed at inducing ovulation. In the patients with PPA the cumulative conception rate was 91% at 12 months from the start of treatment and 98% at 24 months. 80% gave birth to a child by 18 months and 95% by 30 months. These rates were similar to those of the non-PPA group and to previously published normal rates. Hence PPA poses no serious threat to fertility, unlike the tubal damage that may result from use of an IUD. Whatever their previous menstrual history women, especially the nulliparous, who are concerned about their future fertility should be recommended oral contraception in preference to an IUD.
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To evaluate ovulation and pregnancy predictors in infertile polycystic ovary syndrome (PCOS) patients who received clomiphene citrate (CC) and metformin as first-line ovulation inductors.