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The Polycystic Ovary Syndrome (PCOS) is a heterogeneous disorder, whose principal features include androgen excess, ovulatory dysfunction, and/or polycystic ovaries, and is recognized as one of the most common endocrine/metabolic disorders of women. This syndrome was first described by Stein and Leventhal in 1935 [1], although the presence of sclerocystic ovaries had been recognized for at least 90 years before the publication of that seminal work. Following, we review the definition, diagnostic scheme, and epidemiology of PCOS as it currently stands.

Hyperandrogenism, insulin resistance, cardiovascular disease, infertility, cancer, reproduction Polycystic ovary syndrome (PCOS) is a common endocrinopathy in women that in its simplest form consists of unexplained hyperandrogenic chronic anovulation, which affects ~7% of the US population [1]. Because its etiology and natural history are poorly understood, there is controversy about the diagnostic criteria and clinical evaluation of the syndrome. Its origins as a named disorder track back to its original description in the 1930s by Stein and Leventhal, a pair of gynecologists from Chicago, who described a complex of signs and symptoms including oligomenorrhea, enlarged polycystic ovaries, hirsutism, and obesity, and also pioneered the treatment of wedge resection of the ovaries which resulted in more regular menses and improved fertility [2]. Since that time, there has been debate as to what the cardinal features of the syndrome are or should be, but a guiding thread of consensus stemming from this original description has been that this is an ovarian disorder of hyperandrogenism (although whether this is primary or secondary is uncertain) and is most readily diagnosed in women of reproductive age [3, 4]

Candidate gene, association, linkage, single nucleotide polymorphism, haplotype Polycystic ovary syndrome (PCOS) is considered a common, complex genetic disorder, as are conditions such as schizophrenia, asthma, and type 2 diabetes. Such common diseases, including PCOS, appear to have a complex, multifactorial etiology, wherein a variety of predisposing genes, not just one gene, interact with environmental and lifestyle factors to produce disease. Studies in families demonstrated the heritable nature of PCOS itself as well as the component phenotypes of PCOS. This has led to a large number of population studies attempting to discover genes that influence PCOS using the candidate gene approach.

Polycystic ovary syndrome, insulin, signaling pathways, hyperandrogenemia, theca cells, granulosa cells Polycystic ovary syndrome (PCOS) is a common disorder affecting 6–10% of women of childbearing age [1–3]. It is the most frequent endocrine disorder among young women and the principal medical cause of female infertility in North America. It is defined by the presence of hyperandrogenism, chronic anovulation, and/or polycystic ovaries (see Chap. 1 for a fuller discussion of the definition of PCOS), after exclusion of all secondary causes. However, most experts in the field agree that hyperandrogenemia is the central feature of PCOS and probably results from the same ovarian dysfunction that causes oligoanovulation and infertility. Therefore, in this chapter, we will focus on the mechanisms of hyperandrogenemia in PCOS, as this was the most studied characteristic of PCOS in the literature, particularly with respect to insulin actions.

Androgen excess, theca, granulosa, polycystic ovary syndrome, steroidogenesis, folliculogenesis, estrogen, insulin sensitivity, signaling defect. Polycystic ovary syndrome (PCOS) is a common, clinically heterogeneous disorder that affects approximately 6–10% of premenopausal women [1, 2]. Hyperandrogenemia is the biochemical hallmark of PCOS. Reproductive and endocrine abnormalities include disordered gonadotropin secretion, oligomenorrhea and anovulatory infertility, and endometrial hyperplasia. Obesity, hirsutism, acne, and alopecia are often associated with PCOS. The metabolic consequences of PCOS include insulin resistance, lipid abnormalities, and possibly an increased risk of cardiovascular disease [3].

The polycystic ovary syndrome (PCOS), one of the most common causes of hyperandrogenism and chronic oligo-anovulation, affects 4–7% of women [1]. The clinical features of PCOS are heterogeneous and may change throughout the lifespan, starting from adolescence to postmenopausal age. Among other factors, this is largely dependent on the influence of obesity and metabolic alterations, including an insulin resistant state and the metabolic syndrome, which consistently affect most women with PCOS [2].

The management of anovulatory infertility in the polycystic ovary syndrome (PCOS) has traditionally involved the use of clomiphene citrate (CC) and then gonadotropin therapy or laparoscopic ovarian surgery, in those who are clomiphene resistant. There is no clear role for insulin sensitizing and insulin lowering drugs, and algorithms for their place in therapy are still to be agreed upon. Newer therapeutic approaches include aromatase inhibitors and the potential use of in vitro maturation (IVM) of oocytes collected from unstimulated (or minimally stimulated) polycystic ovaries. There has been an unfortunate shift away from monofollicular ovulation induction to the use of in vitro fertilization treatment (IVF), based on a false premise of greater cumulative conception rates and appropriate concerns about multiple pregnancy. Superovulation for IVF presents significant risks for women with polycystic ovaries, namely the potentially life-threatening complication of ovarian hyperstimulation syndrome (OHSS). Carefully conducted and monitored ovulation induction can achieve good cumulative conception rates, and, furthermore, multiple pregnancy rates can be minimized with strict adherence to criteria that limit the number of follicles that are permitted to ovulate.

Polycystic ovary syndrome, economic burden, healthcare cost, diabetes mellitus, cardiovascular disease, dyslipidemia, metabolic syndrome, endometrial cancer The polycystic ovary syndrome (PCOS) results in a number of immediate and long-term morbidities that are associated with a significant impact on quality of life and on economic costs. Immediate morbidities include menstrual dysfunction and abnormal uterine bleeding, subfertility and infertility, and androgen excess-related dermatologic abnormalities including hirsutism, acne, and androgenic alopecia, and an increased risk of obstetrical complications such as pregnancy-induced hypertension and gestational diabetes. However, PCOS is also associated with an increased risk of various other long-term complications or morbidities including cancer, type 2 diabetes mellitus (DM), the metabolic syndrome (MS), and possibly cardiovascular disease (CVD).