Polyendocrine Metabolic Ovarian Syndrome Tổng quan về bệnh

Polyendocrine metabolic ovarian syndrome (PMOS), previously known as polycystic ovarian syndrome, is characterized by hormonal dysregulation that affects weight, metabolic and mental health, skin, and reproductive function. It reflects the underlying endocrine and metabolic pathophysiology, omits the misleading reference to ovarian cysts, and accurately reflects the multisystem nature of the condition. The term intended to support scientific accuracy, clarity, stigma avoidance, and cultural and linguistic appropriateness, and to reduce the risk of delayed diagnosis associated with the term polycystic ovarian syndrome. A co-designed global implementation strategy is under way to support the transition to PMOS, including a transition period, education, and alignment with health systems and disease classification¹.

It is one of the most common endocrinopathies in women of reproductive age and is characterized by menstrual abnormalities and clinical or biochemical features of hyperandrogenism. Incompletely developed follicles are present in the ovaries resulting from anovulation, along with increased ovarian androgen production. In its full presentation, it is accompanied by polycystic ovaries, amenorrhea, hirsutism, and obesity. 

Irregular menstrual cycles may present as: Normal in the first year after menarche during pubertal transition; >1 to <3 years after menarche: <21 or >45 days; >3 years after menarche to perimenopause: <21 or >35 days or <8 cycles/year; >1 year post-menarche: >90 days for any 1 cycle; and primary amenorrhea by 15 years old or >3 years after thelarche (breast development).

If clinical signs of hyperandrogenism (particularly hirsutism) are absent or unclear, assess for biochemical hyperandrogenism to establish polycystic ovarian syndrome and/or phenotype. This may be considered in postmenopausal women with a past diagnosis or long-term history of oligo-amenorrhea with hyperandrogenism and/or polycystic ovarian morphology (PCOM) during the earlier reproductive years (20-40 years old).

¹Accordingly, the term polycystic ovarian syndrome is retained temporarily within this disease management chart, where appropriate, to maintain consistency with source references during the transition period.

The pathogenesis of polycystic ovarian syndrome involves ovarian steroidogenesis and follicular development abnormalities. In polycystic ovarian syndrome, the ovarian follicle does not respond normally to physiologic amounts of follicle-stimulating hormone (FSH), possibly due to impaired interaction between FSH signaling and insulin or insulin-like growth factors (IGFs). Insulin resistance leads to high levels of insulin, bioavailable estradiol, testosterone, and IGF-1, which disrupt hormone production in several tissues. The pituitary gland secretes excess luteinizing hormone (LH) and less FSH, the liver produces less sex hormone-binding globulin (SHBG) and IGF-binding protein 1, the adrenals release more dehydroepiandrosterone sulfate (DHEAS), and the ovaries produce more androstenedione. These changes create a feed-forward cycle that sustains both anovulation and androgen excess.

Biochemical Profile

Polycystic ovarian syndrome results mainly from abnormal ovarian steroidogenesis that may be caused by insulin resistance, leading to hyperinsulinemia. There is increased sensitivity to androgens, and the majority of women have elevated androgen levels. This includes elevated serum concentrations of LH, low to normal FSH, elevated testosterone and androstenedione, low to normal estradiol while estrone level is increased, elevated prolactin, decreased sex hormone-binding globulin, and elevated insulin.

Hyperinsulinemia

Hyperinsulinemia is implicated as the major trigger for disordered ovarian function, disrupted steroidogenesis, and androgen excess. This stimulates androgen secretion by theca cells and also suppresses hepatic production of sex hormone-binding globulin, leading to increased circulating testosterone. Insulin resistance contributes to metabolic dysfunction and may be associated with features of metabolic syndrome that includes dyslipidemia, DM, and increased cardiovascular risk.

Decreased Sex Hormone-Binding Globulin (SHBG)

Decreased sex hormone-binding globulin causes an increase in levels of free active androgens, which accounts for the more marked hirsutism, acne, and other manifestations of hyperandrogenism.

Elevated Estrone

Elevated estrone stimulates hyperplasia of ovarian stroma theca cells, and the unopposed estrogen effects on the endometrium may lead to abnormal uterine bleeding and increased risk of endometrial cancer.