Polycystic ovary syndrome

Abstract

Polycystic ovary syndrome (PCOS) affects 5-20% of women of reproductive age worldwide. The condition is characterized by hyperandrogenism, ovulatory dysfunction and polycystic ovarian morphology (PCOM) - with excessive androgen production by the ovaries being a key feature of PCOS. Metabolic dysfunction characterized by insulin resistance and compensatory hyperinsulinaemia is evident in the vast majority of affected individuals. PCOS increases the risk for type 2 diabetes mellitus, gestational diabetes and other pregnancy-related complications, venous thromboembolism, cerebrovascular and cardiovascular events and endometrial cancer. PCOS is a diagnosis of exclusion, based primarily on the presence of hyperandrogenism, ovulatory dysfunction and PCOM. Treatment should be tailored to the complaints and needs of the patient and involves targeting metabolic abnormalities through lifestyle changes, medication and potentially surgery for the prevention and management of excess weight, androgen suppression and/or blockade, endometrial protection, reproductive therapy and the detection and treatment of psychological features. This Primer summarizes the current state of knowledge regarding the epidemiology, mechanisms and pathophysiology, diagnosis, screening and prevention, management and future investigational directions of the disorder.

An International Consortium Update: Pathophysiology, Diagnosis, and Treatment of Polycystic Ovarian Syndrome in Adolescence

“…Although not mandatory for diagnosis, a hallmark of PCOS is the presence of deregulated secretion of the gonadotropins, LH and FSH, which control ovarian steroidogenesis, follicular dynamics, and ovulation [3, 62-64]. Hence, it is reasonable to hypothesize that altered gonadotropin secretory profiles could impact the cardinal features of PCOS, including hyperandrogenism and ovulatory dysfunction [3, 4].…”

“…Yet, despite decades of research, the etiology of PCOS remains elusive [3]. This collaborative effort, initiated by Pediatric Endocrine Societies, was undertaken because of persistent questions in three areas: pathophysiology, diagnosis, and treatment 1 .…”

The Causes of Infertility, Associated With External Genital Endometriosis and Polycystic Ovary Syndrome

“…Возраст начала, лет 11,645±1,018 [11,[0][1][2][3][4][5][6][7][8][9][10][11][12]0] 13,788±0,927 [13,[0][1][2][3][4][5][6][7][8][9][10][11][12][13][14]0] 10,688±0,693 [10,0-11,0] 12,190±0,981 [12,0-12,0] Количество дней 4, 871±0,885 [4,0-6,0] 3, 333±0,736 [3,0-4,0] 5, 438±0,619 [5,0-6,0] 3, 524±0,512 [3,0-4,0] Длительность МЦ, дни 194±2,428 [25,0-27,0] 32, 455±2,526 [30,0-35,0] 25, 125±1,289 [24,0-26,0] 28, 762±0,995 [28,0-30,0] группе были у двух пациенток (6,06%), не было у 31 пациентки (93,94%). В 3-ей группе был ар-тифициальный аборт у одной пациентки (3,13%), не было у 31 (96,88%), в 4-ой группе артифици-альных абортов не было.…”

Treatment of infertility in women with polycystic ovary syndrome using assisted reproductive technology

“…СПЯ -самая распро-страненная форма гиперандрогенемии у жен-щин репродуктивного возраста, на долю этого заболевания приходится от 72 до 82 % всех слу-чаев недостаточности яичников с избыточной продукцией андрогенов [4]. Женщины с СПЯ составляют около половины больных с эндо-кринным бесплодием [5][6][7]. СПЯ характери-зуется нарушением фолликулогенеза, которое выражается задержкой роста на стадии ма-лых и больших антральных фолликулов, при сoхранении кoличества примoрдиальных фол-ликулов, а также отсутствием инициации до-минантного фолликула и нарушением процесса овуляции [8].…”