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.

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.

Although, ovarian hyperstimulation syndrome (OHSS) is the most serious iatrogenic complication of ovarian stimulation, the condition usually resolves within 14 days in women who are subjected to freeze-all embryos policy; meanwhile symptoms may extend through the first trimester in women who do become pregnant as endogenous human chorionic gonadotropin (hCG) levels continue to stimulate the ovaries. The exact pathophysiology and etiology of OHSS remains unknown, but increased capillary permeability with the resulting loss of fluid into the third space is common to the syndrome [1]. Administration of hCG for final follicle maturation and triggering of ovulation appears to be the pivotal stimulus in a susceptible patient, by releasing vasoactive–angiogenic substances such as vascular endothelial growth factor from the ovaries hyperstimulated with gonadotropins [2].

Prolactin is a polypeptide hormone that was discovered more than 70 years ago and is also known as the lactogenic hormone, lactotropin, luteotropic hormone, or luteotropin [1]. It was initially thought that it is only produced by the anterior pituitary gland and mainly involved with lactation, but increasing evidence suggests that there are other sources of prolactin and that it is involved in diverse essential biological activities [2].

Ovarian hyperstimulation syndrome (OHSS) is the most serious iatrogenic complication of excessive response to ovulation induction or ovarian stimulation during in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) treatment cycles [1–5] The incidence of OHSS has been estimated at 20–33% for mild cases, 3–6% for moderate cases, and 0.1% and 2% for severe cases [6–8]. OHSS is characterized by bilateral, multiple follicular and theca-lutein ovarian cysts (Figure 15.1) and an acute shift in body fluid distribution resulting in ascites (Figure 15.2) and pleural effusion. Rizk and Smitz [9], in an analytical study of the factors that influence the incidence of OHSS, found a wide variation among different centers.

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.