RECOMBINANT LUTEINIZING HORMONE (LH) SUPPLEMENTATION IMPROVES CONTROLLED OVARIAN HYPERSTIMULATION OUTCOME IN WOMEN WITH LOW LH CONCENTRATION DURING MID- AND LATE-FOLLICULAR PHASE

The first attempts at in vitro fertilization (IVF) of human oocytes were performed during cycles utilizing human menopausal gonadotropin (hMG) and human chorionic gonadotropin (hCG). These early cycles resulted in a successful conception, which unfortunately ended as a tubal gestation. The birth of Louise Brown in 1978, the first successful IVF birth, was actually achieved following fertilization during a spontaneous cycle in which ovulation was triggered with endogenous luteinizing hormone (LH).However, due to the greater margin for error afforded by larger numbers of follicles, the practice of IVF rapidly evolved towards the use of controlled ovarian hyperstimulation (COH) to achieve higher pregnancy rates. It is easy to understand why this approach evolved. Oocyte harvesting was accomplished primarily by laparoscopy. Since oocyte yield per follicle was less than 100% and fertilization rates were limited, the relatively traumatic follicle aspiration process was more likely to result in embryo transfer if a greater number of follicles was present.

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PROGESTERONE-INDUCED AUGMENTATION OF PITUITARY GONADOTROPHIN RESPONSES TO LUTEINIZING HORMONE-RELEASING HORMONE IN OESTROGEN-PRE-TREATED AMENORRHOEIC WOMEN

Acta Endocrinologica ◽

10.1530/acta.0.0830684 ◽

1976 ◽

Vol 83 (4) ◽

pp. 684-691 ◽

Cited By ~ 3

Author(s):

Sven Johan Nillius ◽

Leif Wide

Keyword(s):

Luteinizing Hormone ◽

Follicle Stimulating Hormone ◽

Follicular Phase ◽

Reserve Capacity ◽

Serum Progesterone ◽

Luteinizing Hormone Releasing Hormone ◽

Releasing Hormone ◽

Before And After ◽

The Mean ◽

Late Follicular Phase

ABSTRACT Modulating effects of oestradiol-17β and progesterone on the pituitary responsiveness to luteinizing hormone-releasing hormone (LRH) were investigated in 12 women with functional amenorrhoea. The pituitary reserve capacity for gonadotrophin section was investigated with repeated intravenous LRH tests before and after administration of oestradiol-1β followed by either progesterone or saline. Intramuscular injection of 1 mg of oestradiol-17β benzoate resulted in a suppression of both the basal gonadotrophin levels in serum and the gonadotrophin responses to LRH 24 h later. Progesterone, 25 mg im, was then administered in eleven experiments. Six h later, when the mean serum progesterone level had increased to levels similar to those seen in the early post-ovulatory phase of the menstrual cycle, there was a marked augmentation of the pituitary capacity to release both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in response to LRH. This was not found in eight experiments where saline was given instead of progesterone after oestrogen pretreatment. These findings suggest that the greatly increased pituitary sensitivity to LRH at midcycle may be caused not only by the oestradiol increase in blood during the late follicular phase but also in part by the small pre-ovulatory rise of progesterone during the mid-cyclic LH peak. Furthermore, they add further support to the hypothesis that progesterone as well as oestradiol is involved in the induction of the LH peak at midcycle. Progesterone may be of importance to secure the release of enough LH for ovulation and normal corpus luteum formation to occur.

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