Induction of ovulation with low-dose gonadotropins in polycystic ovary syndrome: an analysis of 109 pregnancies in 225 women.

White, Davinia; Polson, D. W.; Kiddy, D.; Sagle, P; Watson, H.; Gilling-Smith, Carole; Hamilton‐Fairley, Diana; Franks, Stephen

doi:10.1210/jcem.81.11.8923819

Cited by 85 publications

(80 citation statements)

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“…85 Accordingly, the pregnancy rate after a low-dose human menopausal gonadotropin (hMG) or pure FSH administration may be significantly lower in obese than in normal-weight PCOS women. 86 Finally, in recent studies on PCOS women conceiving after in vitro fertilization or intracytoplasmatic sperm injection, it was observed that those with obesity had higher Obesity and the polycystic ovary syndrome A Gambineri et al gonadotrophin requirement during stimulation, 87 fewer oocytes, a higher abortion rate and lower live-birth rate than their non-obese counterpart. 88 In conclusion, a decreased efficiency of the different treatments for ovulation and fertility induction may be expected in obese PCOS women.…”

Section: Androgen Abnormalitiesmentioning

confidence: 99%

Obesity and the polycystic ovary syndrome

et al. 2002

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The polycystic ovary syndrome (PCOS) is a condition characterized by hyperandrogenism and chronic oligo-anovulation. However, many features of the metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are overweight or obese and most of them have the abdominal phenotype. Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and, possibly, high dietary lipid intake, may be additional mechanisms by which obesity favours the development of hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype.Body weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and=or antiandrogens to weight reduction programmes. These obviously emphasize the role of obesity in the pathophysiology of PCOS.

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Section: Androgen Abnormalitiesmentioning

confidence: 99%

Obesity and the polycystic ovary syndrome

et al. 2002

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“…There were more mature oocytes, embryos cleaved, increased fertilisation and clinical pregnancy rates [70% vs 30%] in the metformin group [53]. These latter two studies would seem to confirm that both obese [12] and insulin resistant [10] women with PCOS have a much greater tendency to a multifollicular response and thus a relatively high cycle cancellation rate on low dose FSH stimulation.…”

Section: Metforminmentioning

confidence: 76%

“…Obese women being treated with low dose gonadotrophin therapy have inferior pregnancy and miscarriage rates [11]. Both obese [12] and insulin resistant [10] women with PCOS, even on low dose FSH stimulation, have a much greater tendency to a multifollicular response and thus a relatively high cycle cancellation rate in order to avoid hyperstimulation.…”

Section: Weight Lossmentioning

confidence: 99%

“…[38] Assuming that the step-up protocol is superior to the stepdown version, do the initial dose, the duration of its administration and the incremental dose rise influence results? From the largest published series of chronic low dose FSH therapy [12] it was possible to compare the results of a starting dose of 75 IU with that of 52.5 IU for an initial 14-day period with an incremental dose rise of 37.5 IU or 22.5 IU respectively. There were no significant differences between the two groups but pregnancy rate/ patient, uni-ovulatory cycle rate and miscarriage rate were all in favour of the smaller starting dose.…”

Section: Gonadotrophin Therapymentioning

confidence: 99%

“…Although the majority of patients with PCOS will reach criteria for hCG administration within 14 days using 75 IU/day of urinary FSH [12] or 50 IU/day of recombinant FSH, some have attempted to cut down the initial period of 14 days without change of dose to 7 days. A comparison of 14 day versus 7 day starters [31] in 50 patients showed no significant differences other than a slightly higher rate of multiple pregnancies in the 7-day group.…”

Section: Gonadotrophin Therapymentioning

confidence: 99%

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Long-term sequelae of polycystic ovary syndrome: diabetes and cardiovascular disease

2005

Polycystic Ovary Syndrome

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Polycystic ovary syndrome [PCOS] is the commonest cause of anovulatory infertility. Treatment modes available are numerous mainly relying on ovarian stimulation with FSH, a reduction in insulin concentrations and a decrease in LH levels as the basis of the therapeutic principles. Clomiphene citrate is still the first line treatment and if unsuccessful is usually followed by direct FSH stimulation. This should be given in a low dose protocol, essential to avoid the otherwise prevalent complications of ovarian hyperstimulation syndrome and multiple pregnancies. The addition of a GnRH agonists, while very useful during IVF/ET, adds little to ovulation induction success whereas the position of GnRH antagonists is not yet clear. Hyperinsulinemia is the commonest contributor to the state of anovulation and its reduction, by weight loss or insulin sensitizing agents such as metformin, will alone often restore ovulation or will improve results when used in combination with other agents. Laparoscopic ovarian drilling is proving equally as successful as FSH for the induction of ovulation, particularly in thin patients with high LH concentrations. Aromatase inhibitors are presently being examined and may replace clomiphene in the future. When all else has failed, IVF/ET produces excellent results. In conclusion, there are very few women suffering from anovulatory infertility associated with PCOS who cannot be successfully treated today. ReviewPolycystic ovary syndrome [PCOS] is associated with approximately 75% of women who suffer from infertility due to anovulation [1,2]. It is a very heterogeneous syndrome both in its clinical presentation and laboratory manifestations. The majority of women with anovulation due to PCOS have menstrual irregularities, usually oligomenorrhea or amenorrhea, associated with clinical and/or biochemical evidence of hyperandrogenism. The main disturbances in this syndrome are:1. Abnormal morphology of the ovary, detected by a characteristic hyperechogenic enlarged central stroma and >9 small follicles of 2-9 mm diameter on transvaginal ultrasound examination of the ovaries [3].2. Abnormal steroidogenesis, mainly increased ovarian production of androgens but also increased progesterone and estradiol production.3. Hyperinsulinemia, present in about 80% of obese women and 30-40% of women of normal weight with PCOS [4] and more strongly associated with anovulation than any other feature of the syndrome.

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