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Polycystic ovary syndrome (PCOS) is a complex endocrinologic disorder resulting in chronic anovulation. The clinical appearance of PCOS was originally described by Stein and Leventhal in 1905 (often called the Stein Leventhal syndrome) and classically has involved obesity (overweight), amenorrhea (absence of menstrual flow) and hirsutism (excess hair growth with a male pattern) associated with the finding of enlarged ovaries that have many follicular cysts seemingly arrested in development. PCOS is a relatively common disorder of chronic anovulation. It (PCOS) typically results in (very) irregular menstrual intervals from the time of puberty onward. PCOS has an endocrinologic (hormonal) basis associated with an increased (hypothalamic) GnRH (gonadotropin releasing hormone) pulse amplitude (increased amount of released hormone per pulse), tonically elevated levels of LH, and suppressed levels of FSH to result in a classically elevated LH:FSH ratio (about 2.5 or greater). When women with PCOS have GnRH administered (in research) to them there is an exaggerated LH (but not FSH) response. There is usually an elevated concentration of ovarian androgens (androstenedione and testosterone) thought to be due to the elevated LH (which promotes production of these hormones in the ovary). There is also (often) an increased concentration of circulating adrenal androgens such as DHEAS (adrenal gland stimulation of androgen production with adrenocorticotropic hormone [ACTH] appears to be exaggerated while circulating concentrations of ACTH are normal in PCOS women). Therefore, some authorities have described PCOS as a condition of “hyperandrogenic chronic anovulation.” The androgenic hormones are the ones that produce the “male pattern” alterations, such as acne, oily skin, excess (male pattern) hair growth, and (male pattern) obesity. It is thought that PCOS women without excess (male pattern) hair growth (about 30% of PCOS women) may have a deficiency in the enzyme (5-alpha reductase) that converts the androgenic hormones into their more bioactive counterparts (such as dihydrotestosterone). It is the dihydrotestosterone that promotes the transition from vellous hair (soft, fine, unpigmented, “female” hair) to terminal hair (course, thick, pigmented, “male” hair) to produce the appearance of “male pattern” hair growth. Many women with PCOS have a mild elevation of insulin and associated insulin resistance. Obese women have a greater disorder of insulin than thin women. Research suggests that hyperinsulinemia (elevated circulating concentratrations of insulin) with impaired glucose tolerance occurs predominantly in obese (heavy) PCOS women. There is also a syndrome called HAIR-AN syndrome, which involves hyperandrogenic insulin resistance and acanthosis nigricans. Acanthosis nigricans is an irregular velvety dark discoloration of the skin especially in regions of skin folds or creases. It seems to be especially difficult to stimulate ovulation in women with HAIR-AN syndrome. The cause of PCOS is not known. Regardless of the cause, PCOS is characterized by a vicious cycle of endocrinologic events involving the ovaries, adrenal glands, pituitary gland and hypothalamus. | |
