Deficiencies in luteal hormonal dynamics have been clearly documented during controlled ovarian stimulation [1]. Disruptions to the physiological secretion of luteinizing hormone (LH) by the anterior pituitary affect optimal corpus luteum (CL) function warranting some form of luteal phase support (LPS) in order to maintain optimal endometrial receptivity in stimulated cycles.

Half a decade ago, we witnessed the culmination of much of what we comprehend today in classical ovarian endocrinology and physiology [1;2], human embryology [3] as well as clinical ovarian ultrasonography [4]. Much of the former was based upon the development of (radio-)immunoassays that could reliably detect low concentrations of hormones in body fluids, including the peripheral circulation. This meant that correlations of hormone concentrations and specific physiological events could be determined with precision, leading to many advances in clinical practice and drug development. The biological control of all these physiological elements is, of course, gonadotropin-releasing hormone (GnRH), whose decapeptide structure was elucidated by Andrew Schally and colleagues in 1971 [5], for which he was awarded his share of the Nobel prize in 1977. His co-prize winners were responsible for the pioneering of immunological competitive binding dilution assays, which underwrote all these developments.

Traditionally, controlled ovarian stimulation in women undergoing assisted reproductive technology (ART) treatment was designed in a standardized fashion taking into account the age and body weight of the patient. A standardized treatment protocol has been described as a “one-size-fits-all” approach that does not take into account inter-individual differences.

Polycystic ovarian syndrome (PCOS) is one of the most prevalent endocrinopathies affecting 5 to 10 percent of women of reproductive age [1;2]. Characteristic clinical features of PCOS include menstrual irregularity such as oligomenorrhea/amenorrhea and signs of hyperandrogenemia including hirsutism, acne, and/or obesity. The syndrome was first clearly described by Stein and Leventhal in 1935 [3]. While the primary etiology remains poorly defined [4], insulin resistance with compensatory hyperinsulinemia is a prominent feature of the condition and appears to be an underlying cause of hyperandrogenemia identified in both lean and obese women [5]. Hyperinsulinemia promotes increased ovarian androgen biosynthesis in vivo and in vitro [6;7]. It also decreases sex hormone-binding globulin production in the liver [8], which results in the increased bioavailability of free androgens and exacerbates the signs of androgen excess.

Reproduction in humans is contingent upon the pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus. This neuroendocrine activity results in the production and release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and is essential therefore for proper steroidogenesis and gametogenesis within gonads.

Gonadotropin-releasing hormone (GnRH) is secreted from the medial basal hypothalamus and controls pituitary function via the hypothalamic tuberoinfundibular system [1]. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are synthesized and secreted by the anterior pituitary gland in response to GnRH pulse activity. Physiological modulation of GnRH pulse amplitude and frequency determines the fine interplay between various gonadotropin players during the menstrual cycle [2;3].

Surgical methods of ovulation induction for women with clomiphene (clomifene) citrate-resistant polycystic ovary syndrome (PCOS) include laparoscopic ovarian drilling with diathermy. This technique has replaced the more invasive and damaging technique of ovarian wedge resection first introduced by Gjønnaess in the early 1980s [1]. Laparoscopic ovarian surgery is free from the risks of multiple pregnancy and ovarian hyperstimulation, which makes it an attractive procedure for PCOS women, but surgery is not without risks. The techniques of laparoscopic ovarian diathermy have been described previously [2;3]. Studies suggest that four punctures per ovary with application of diathermy current via needle cautery set at 30 watts for 5 seconds per puncture (i.e., no more than 600 J per ovary) should produce an optimal response. The greater the damage to the surface of the ovary the greater the risk of peri-ovarian adhesions estimated at 60 percent (ranging from 0 to 100 percent) in treated women.