Polycystic ovarian syndrome (Stein-Leventhal syndrome) is a complex endocrine disorder affecting women in their reproductive years.
It is characterized by increased androgen production and disordered gonadotropin secretion, which results in chronic anovulation.
It is the leading cause of anovulatory infertility and hirsutism.
PCOS is also associated with disorders of reproduction, metabolism, and general health, including increased risk of miscarriage, insulin resistance, hyperlipidemia, cardiovascular disease, and endometrial cancer.
Obesity is common but not universal in women with PCOS.
Women with PCOS have high rate of type 2 diabetes; these women have hyperlipidemia and a greatly increased risk of cardiovascular disease.
Most common cause of infertility in women
Classic syndrome originally described by Stein and Levanthal
Syndrome, not a disease—multiple potential etiologies with variable clinical expression
Why is PCOS important?
Affects 4-12% of women of reproductive age
Significant association between obesity, insulin resistance, and PCOS.
Huge impact on the reproductive, metabolic, and cardiovascular health of affected women.
Clinical Features of PCOS Menstrual Irregularity
May appear at puberty with a delayed menarche followed by the onset of irregular periods or as the breakdown of a previously regular cycle
Anovulation is usually chronic and presents as oligomenorrhea or amenorrhea
Clinical Features of PCOS Hyperandrogenism
Symptoms may include hirsutism, acne, male pattern balding, and/or male distribution of body hair
2. Insulin resistance
Common Endocrine Abnormalities in PCOS
Elevated luteinizing hormone (LH)
Increased LH/follicle-stimulating hormone (FSH) ratio
Elevated androgen levels
Decreased sex hormone binding globulin levels
In PCOS, discovered increased pulse frequency of GnRH (2/2 abnml pulse generator), resulting in relatively increased pulse frequency of LH, over FSH.
Increased frequency of LH pulses in PCOS. Progesterone administration can restrain rapid pulse frequency. Increased LH results in increased production of androgens by ovarian theca cells.
INSULIN acts synergistically with LH to enhance androgen production. INSULIN suppresses SHBG (the key protein that binds testosterone), resulting in increased free testosterone.
TESTOSTERONE inhibits and estrogen stimulates hepatic synthesis of Sex hormone-binding globulin (SHBG).
Symptoms of androgen excess
Reduced sex-hormone-binding globulin (SHBG) more free testosterone conversion of androstenedione in adipose tissue
Metabolic Abnormalities in PCOS
Hyperinsulinemia and insulin resistance
Insulin resistance may be independent of the effect of obesity
Decreased peripheral insulin sensitivity and consequent hyperinsulinemia may play an important role in the pathogenesis of PCOS