Sunday, December 10, 2023
This activity is intended for primary care clinicians, gynecologists and obstetricians, and other specialists who care for women.
The goal of this activity is to update clinicians on the pathophysiology of polycystic ovary syndrome and describe the range of clinical manifestations of the condition.
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The symptoms of women with polycystic ovary syndrome (PCOS) include hirsutism and irregular menstrual bleeding due to ovarian androgen excess and chronic anovulation. Typically, these features emerge late in puberty or shortly thereafter. The proposed mechanism(s) responsible for increased ovarian androgen production include heightened theca cell responsiveness to gonadotropin stimulation, increased pituitary secretion of luteinizing hormone, and hyperinsulinemia. The cause of ovulatory dysfunction is not well understood, but is linked to abnormal follicle growth and development within the ovary. As a result, infertility is common among women with PCOS and, in many instances, is the initial presenting complaint. Insulin resistance and obesity are frequently associated with PCOS and probably contribute to the severity of symptoms. The polycystic ovary that accompanies the syndrome has recently been defined as having 12 or more follicles per ovary or an ovarian volume greater than 10 ml as determined by ultrasonography. In addition, there is an increased number of growing follicles in the polycystic ovary. Despite this distinctive appearance, the cause and development of the polycystic ovary are completely unknown.
The primary clinical manifestations of polycystic ovary syndrome (PCOS) are hirsutism and irregular menstrual bleeding due to ovarian androgen excess and chronic anovulation. The prevalence of PCOS in hirsute women is approximately 75%, whereas the frequency in women with irregular bleeding ranges from 75% to 90%.[1,2] Commonly, these features emerge late in puberty or shortly thereafter. In addition, the disorder has been inseparably linked to specific morphological changes of the ovary.
The presence of insulin resistance in 50–70% of cases, or obesity in about 60%, seems to further amplify the severity of the condition at presentation.[3] The prevalence of obesity in PCOS in the United States is greater than rates observed in other countries.[4,5] The physiologic alterations of PCOS seem to arise primarily from abnormal ovarian steroidogenesis as a consequence of inappropriate hypothalamic–pituitary–ovarian interaction. The relationship between ovarian dysfunction and the morphogenesis of the ovary is, however, not well understood. In this article, the clinical manifestations of PCOS are described with respect to the mechanisms that seem to underlie the altered reproductive physiology. In particular, the roles of androgens, gonadotropins, insulin, estrogens, and obesity are emphasized.
